By contrast, translocation of the virulence factor CagA leads to extracellular signal-regulated kinase ERK and mitogen-activated protein kinase MAPK phosphorylation and induction of the anti-apoptotic protein B cell lymphoma 2 BCL-2 , thereby preventing B cell death 87 , Manipulation of B cell survival by parasites. Both Trypanosoma brucei and T.
In mice, T. Similarly to Trypanosoma spp. However, whether B cell death occurs owing to direct contact with Trypanosoma spp. Interestingly, T. These parasites also induce the dilution of antibody responses, and their effect on B cells seems to be dependent on the B cell subpopulation that is targeted. Therefore, Trypanosoma spp. Manipulation of B cell survival by viruses. Viruses that cause the development of B cell lymphomas often have the capacity to directly increase B cell survival 59 , 78 , 79 Table 1.
Whereas EBV persists intracellularly in B cells, where it hides from antibody responses, HCV can induce non-protective antibody responses and lymphoproliferative disorders. These two viruses provide an intriguing example of how the induction of B cell survival can facilitate infectious processes. In contrast to viruses that induce B cell survival, influenza A virus leads to the induction of B cell death.
Mouse B cells carrying a BCR specific for influenza haemagglutinin were found to be infected in vitro and in vivo in the lungs, failed to produce antibodies and ultimately died These data suggest that targeting of antigen-specific B cells at the infectious site could be an efficient mechanism to impair or delay the adaptive immune response to infection.
Manipulation of B cell survival by bacteria. Similarly to viruses and parasites, bacterial pathogens can manipulate the survival and cell death pathways of B cells Table 1. For example, Listeria monocytogenes infection results in high cytotoxicity for B cells. Interestingly, L. Apoptosis of B cells in vitro has also been described following infection with Francisella tularensis Similarly to F.
Interestingly, induction of apoptosis in uninfected B cells requires a functional T3SS, but is independent of the translocation of T3SS-dependent virulence effectors. Instead, the virulence effector IpaD — the needle-tip protein of the Shigella spp.
The presence of an as yet unidentified bacterial co-signal or multiple co-signals is necessary for the triggering of IpaD-mediated cell death, as apoptotic B cells were only detected when cells were co-incubated with IpaD and non-pathogenic S. Notably, the co-incubation with non-pathogenic bacteria results in the loss of both mitochondrial membrane potential and the upregulation of mRNA encoding TLR2. Shigella spp. Helicobacter pylori infection has also been shown to lead to translocation of AIF and induction of apoptosis in a B cell line, which has been associated with the persistence of H.
By contrast, translocation of the H. Whereas the induction of apoptosis has been suggested to facilitate persistence by deletion of protective B cells, the increased survival of B cells has been associated with H. Whether one or both of these mechanisms occur in vivo in infections with H. In contrast to bacteria that induce B cell death, S.
Typhimurium induces B cell survival, which has been suggested to benefit the bacterium as it uses B cells as a survival and dissemination niche Notably, S. Typhimurium infection, which prevents activation of the inflammasome and the induction of cell death Interestingly, inhibition of the inflammasome occurs in both infected and uninfected cells and requires the S.
Together, these studies highlight that pathogens can interfere with both survival and cell death pathways in B cells. Interestingly, pathogens that use B cells as a niche for survival or dissemination or that divert B cell maturation often increase B cell survival, presumably to facilitate their persistence in the host.
Acute, recurrent infections, however, are often accompanied by B cell death and impaired protective immune responses, suggesting that reinfection is facilitated by the deletion of the cell population that confers protective immunity. Increasing evidence is emerging that several pathogenic parasites, viruses and bacteria interact directly with and manipulate B cells. Such direct targeting, in addition to the indirect effect of the infection-induced local microenvironment, illustrates the diversity of mechanisms used by pathogens to evade host protective immunity.
Pathogens manipulate B cells using three main strategies: the use of B cells as a reservoir, the diversion of B cell maturation either by the induction of short-lived plasma cells that secrete antibodies of low specificity or by the induction of immunosuppressive regulatory B cells , and the modulation of B cell survival. Interestingly, some pathogens use multiple mechanisms simultaneously to ensure their survival. For example, several viruses that cause persistent infections induce B cell survival, which can result in lymphoma formation.
Although it seems detrimental to the viruses to induce the survival of B cells, these viruses have often found ways to hide from or subvert the antibody response in order to persist within the host.
By contrast, in the case of acute infections or host-restricted pathogens, pathogens have evolved mechanisms to facilitate reinfection. For instance, by inducing B cell death, S. Typhimurium suppresses immune responses by a different mechanism involving the induction of regulatory B cells, which modulate protective responses mediated by T cells and other innate immune cells 16 , Regulatory B cells have received increasing attention and are also induced in several viral and parasitic infections.
Although these cells show therapeutic potential in the treatment of autoimmune diseases, further insight into the mechanisms by which regulatory functions are triggered is needed to provide information on how to prevent their detrimental effects following infections.
To elucidate cellular mechanisms of B cell manipulation by pathogens, a combination of in vitro and in vivo studies seems particularly promising.
For instance, a recent study using human and mouse norovirus strains elegantly shows that B cells provide a cellular target for the virus in vitro and in vivo , and that infection is promoted by enteric bacteria expressing histo-blood group antigen Notably, pathogens are often used as a simple tool for deciphering the generation of immune cell functions, but recent evidence highlights their ability to divert immune responses by expressing key virulence factors.
New approaches are thus needed to gain insights into the role of such weapons in infections. For instance, a fluorescence resonance energy transfer FRET -based assay to directly monitor the delivery of virulence effectors into host cells was recently used to investigate whether B cells are deliberate targets of T3SS-bearing bacteria in vitro and in vivo 91 , 92 , 93 , The identification of key virulence factors diverting host responses could also affect vaccine design, especially for live attenuated vaccine candidates, which involve the identification and deletion of virulence factors that have a negative effect on the host-protective immune responses.
For example, the S. The recent demonstration that IpaD induces B cell death, but only in the presence of bacterial cofactors 41 , suggests that IpaD-specific antibodies elicited upon immunization would not only prevent cell invasion but also the induction of B cell death triggered during infection. Therefore, an IpaD-based subunit vaccine seems particularly promising in the fight against S.
Additionally, systems biology approaches targeted at detecting infection and vaccination signatures in people may help us to gain insights into how protective immune responses are established. For example, systems analysis and bioinformatics integration of various 'omics' approaches, in combination with traditional experimental approaches, have contributed to a better characterization of the host immune response against West Nile virus infection To combine such an analysis with insights into manipulation strategies used by pathogens would substantially increase our knowledge of how protective B cell responses are elicited and diverted during particular infections, which may lead to novel therapeutic and vaccination approaches in the future.
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Leukocyte Biol. This review describes both positive and negative effects of polyclonal B cell activation on the protective immune response during infections.
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Dang, V. From the regulatory functions of B cells to the identification of cytokine-producing plasma cell subsets. This review summarizes current knowledge on regulatory B cells and argues that several subsets of antibody-producing plasma cells are able to secrete immune-regulatory cytokines.
Shen, P. ILproducing B cells are critical regulators of immunity during autoimmune and infectious diseases. Bermejo, D. This publication provides the first mechanistic details on the induction of IL during a pathogenic infection, identifying both the virulence factor and the B cell signalling pathway involved. Weiss, G. The Plasmodium falciparum -specific human memory B cell compartment expands gradually with repeated malaria infections.
PLoS Pathog. By comparing the protective immune response to malaria infection with a tetanus vaccine, this publication shows that the induction of B cell antibody production can be diverted during pathogenic infections.
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McChesney, M. Measles virus infection of B lymphocytes permits cellular activation but blocks progression through the cell cycle. Shannon-Lowe, C. Epstein Barr virus entry; kissing and conjugation. Borza, C. Alternate replication in B cells and epithelial cells switches tropism of Epstein-Barr virus. Nature Med. Babcock, G. EBV persistence in memory B cells in vivo.
Immunity 9 , — B cells under influence: transformation of B cells by Epstein—Barr virus. This review summarizes current knowledge on the interaction of EBV with B cells, including the use of particular virulence factors to subvert B cell function. Karapetian, O. Retroviral infection of neonatal Peyer's patch lymphocytes: the mouse mammary tumor virus model.
Held, W. Superantigen-induced immune stimulation amplifies mouse mammary tumor virus infection and allows virus transmission. Cell 74 , — Golovkina, T. B and T cells are required for mouse mammary tumor virus spread within the mammary gland. Finke, D. Typhimurium in mouse is very similar to that caused by Salmonella Typhi in the human, and much of the knowledge of this infection is due to studies in the murine model with S.
Typhimurium [ ]. Salmonella are facultative intracellular pathogens; both serovars share many virulence factors flagella, lipopolysaccharide, and pathogenicity islands but differ in clinical manifestations: typhoid fever occurs within 2 weeks and has systemic manifestations, and gastroenteritis occurs in a shorter period 12—72 h , with a rapid accumulation of neutrophils at the intestinal level [ ].
After S. Once internalized, Salmonella resides intracellularly in membranes called Salmonella -containing vacuole SCV , which protects the bacteria by avoiding fusion with lysosomes and avoiding the reactivity of reactive oxygen metabolites [ , ].
Salmonella can infect several cell types, from macrophage and dendritic cells to non-phagocytic like epithelial cells and hepatocytes [ ]. Salmonella can be internalized in and infect B lymphocytes [ 43 ].
Evidence has shown that Salmonella is internalized into B lymphocytes through a macropinocytosis process [ 72 , 73 ]. Depending on the internalization mechanism, Salmonella survival will occur, for instance, bacteria opsonized with complement or internalized by a mechanism triggered by products of the SPI-1 survive a replicate few hours after internalization, whereas bacteria opsonized with IgG or not opsonized will be eliminated soon after internalization [ ].
Once internalized, the bacterium resides in SCV vacuoles, which in the case of B lymphocytes allow the cross-presentation of the Salmonella antigens to major histocompatibility complex molecules class one MHC-I , by the vacuolar or cytosolic pathways [ ]. One of the characteristics of Salmonella is its ability to persist, and the use of the PD1 system in B lymphocytes makes them an ideal niche for prolonged stay in the body.
The genus Mycobacterium comprises a large number of species, some of which are highly pathogenic as Mycobacterium tuberculosis MTB , being also the most studied species of all mycobacteria. MTB is a facultative intracellular pathogen; macrophages are the main cells where the mycobacteria reside and multiply [ ], being able to infect other cells such as pulmonary epithelial cells [ 93 , ], fibroblasts [ ], adipocytes [ ], or endothelial cells [ ]; bacterial replication into the non-phagocytic cells is discrete, so they have been suggested as niches where the bacteria may persist.
In mycobacterial infections, the protective response is cellular, mediated by T helper Th lymphocytes and activated macrophages [ ]. The involvement of antibodies and B lymphocytes has recently begun to be recognized. For example, B lymphocytes are required to control pulmonary inflammation and bacterial load [ ] and antibodies and cytokine production by B lymphocytes mainly IL and contribute to these activities [ ]. Lymphocytes have been considered as non-phagocytic cells or with less interiorization capacity than macrophages [ 70 , 71 ].
Mycobacteria promote their internalization in non-phagocytic cells, including B lymphocytes [ 72 ]. One way to establish the low phagocytic activity of B lymphocytes is to incubate them in the presence of inert particles like zymosan Figure 4.
B cells from the Raji cell line were incubated with zymosan without any further treatment, during 3 h; then cells were fixed with paraformaldehyde and stained with Giemsa dye. Control cells: cells did not receive any treatment. Zymosan only: cells were incubated with zymosan without any treatment. Zymosan and MTB SN: cells were incubated with zymosan and Mycobacterium tuberculosis filtrated growth bacterial culture medium 0.
Zymosan only: zymosan particles were observed bound to B-cell membrane; 3 h after, zymosan was not observed into the B cells. Macropinocytosis is an internalization process triggered by several inductors [ ]; experimentally, phorbol esters trigger macropinocytosis even in phagocytic cells [ ]. Pathogens use this internalization mechanism to achieve their entry into cells, by producing factors that trigger cytoskeleton reorganization [ 93 ]; for the case of mycobacteria, our group has suggested that pathogenic mycobacteria such as M.
Some of the reported mycobacterial products that facilitate adhesion and internalization into non-phagocytic cells are fibronectin-binding protein FBP and heparin-binding hemagglutinin adhesin HBHA [ , ], among others [ , ]. The internalization of mycobacteria in immortalized B lymphocytes cell lines has been described by some authors [ 72 , 74 , ]; these studies show that M. There are scarce studies on human in vivo B-lymphocyte infection [ ], so establishing the precise involvement of B lymphocytes in mycobacterial infections is an area of great interest.
B-cell membrane changes after 1 h of incubation with PMA or mycobacteria derivatives. Panel a Control cells. Panel b Cells treated with phorbol-myristate-acetate PMA , a classical macropinocytosis inductor. Panel c Cells treated with filtrated supernatant from growth culture medium of Mycobacterium smegmatis. Panel d Cells infected with Mycobacterium tuberculosis.
Fluorescence images correspond to actin cytoskeleton labeled with phalloidin rhodamine. B lymphocytes are involved in various stages of the immune response against pathogens; the traditional role of these cells has been associated with adaptive immune response, characterized by the production of antibodies and the generation of immune memory.
In bacterial infection, the role of these cells in the innate response has recently been recognized; in this sense, it has been demonstrated that B cells express receptors capable to recognize bacterial structures TLRs, CR, dectin-1, etc. The immune response induced in B lymphocytes often depends on the type of pathogen and the way in which B cell is activated, so B-cell response may be regulated by the bacteria to favor its intracellular survival.
The B lymphocytes possess an endocytic capability that allows them to internalize pathogens; the mechanisms that these cells use to internalize bacteria can be endocytosis dependent or independent of clathrin, macropinocytosis, phagocytosis, etc. As a result of this internalization, B lymphocytes produce a series of mediators of the innate response that will be described.
B-cell plasticity is so extensive that any of these profiles can be induced by B cells depending on how they are activated [ — ]. Although B cells can show an inflammatory profile in response to bacterial infections, they cannot control infection at all times; some pathogens, especially intracellular ones, are able to occupy B cells as reservoirs of infection and can modulate the immune response of these cells to survive or even multiply within B lymphocytes.
In the case of B-lymphocyte interaction with some Gram-negative bacteria such as Brucella abortus [ 69 ], M. Listeria monocytogenes infection shows an ILproducing B-cell profile at very early stages of infection, which promotes bacteria persistence and dissemination [ — ]. Another example of B lymphocyte-bacteria interaction is the infection caused by F. Nitric oxide is one of the important mediators of the immune response that plays a fundamental role in the elimination of pathogens.
This molecule is produced by classical phagocytic cells; however, its production has also been described by cells classified as non-phagocytic including B lymphocytes. During respiratory burst, NO in conjunction with the reactive oxygen species ROS participates in the formation of peroxynitrites, which are highly oxidizing agents of many components of the bacteria.
NO increases its expression and activity in B lymphocytes infected with intracellular pathogens such as M. Typhimurium , and Citrobacter rodentium [ — ]. The subclass of B1 lymphocytes constitutively produces nitric oxide inducible synthase iNOS ; however, in infectious events this enzyme increases its expression levels and therefore its activity, such as the LBs infected with Cryptococcus neoformans ; in this infection, NO has a fundamental role in the elimination of the pathogen [ ].
NO production in B1 lymphocytes appears to be linked to the stimulation of various TLRs, since some studies have shown that the stimulation of these receptors and their ligands resulted in production of higher NO levels by B lymphocytes. Antimicrobial peptides are innate response effectors present in most human cells; these molecules are classified into alpha-defensins HNP beta-defensins hBD , and cathelicidins such as LL Its mechanisms of action include the direct lysis of the microorganisms, the generation of a proinflammatory environment, or the modulation of the immune response.
There are very few studies on B-lymphocyte expression of antimicrobial peptides; however, there are some evidences demonstrating that B cells express antimicrobial peptides in constitutive and inducible fashion; under stimulation with some PAMPS, B lymphocytes express alpha defensins HNPs 1—3 , hBD2, and the cathelicidin LL [ , ]. B cells participate actively in the control of microorganisms, and although many authors have considered them as non-phagocytic cells, it seems that these cells possess microbicidal capacities, since they are able to produce antibacterial mediators like ROS.
The Nox family of enzymes is responsible for regulating the production of ROS in several cell types like neutrophils and macrophages; the Nox2 isoform is particularly essential in the elimination of bacteria in these cells. Recently Nox2 production was described by splenic and peritoneal B lymphocytes; the absence in Nox2 production decreases the production of ROS resulting in a deficient elimination of Staphylococcus aureus by B lymphocytes; contrarily normal B cell controlled intracellular bacteria growth [ ].
The ability of several pathogens to regulate the death pathways of the host cell has been described for most of the pathogens that infect different cells, and actually this situation is recognized for B lymphocytes. For example, L. The fourth family has only one member lymphotoxin XCL1 ; this chemokine is similar to members of the CC and CXC families, but the lack of two of the four cysteine residues are characteristic of this chemokine. Its chemotactic function is for lymphocytes and not for monocytes and neutrophils as do other chemotactic chemokines [ ].
Inflammation is a protective response to extreme challenges to homeostasis, such as infection, tissue stress, and injury [ ], which is characterized by its cardinal signs: redness, swelling, heat, pain, and disrupted function [ ]. A typical inflammatory response consists of four components: 1 inflammatory inducers: depending on the type of infection bacterial, viral, fungi or parasitic [ ]; 2 sensors that detect the inflammatory inducers: these sensors are receptors of the innate immune system such as TLRs, NLRs and RLRs [ , ]; 3 inflammatory mediators induced by the sensors, such as cytokines, chemokines and the complement system [ ]; 4 target tissues that are affected by the inflammatory mediator.
Each component comes in multiple forms and their combinations function in distinct inflammatory pathways. The inflammatory reaction is characterized by successive phases: 1 silent phase, where cells reside in the damaged tissue releases in the first inflammatory mediators, 2 a vascular phase, where vasodilation and increased vascular permeability occur, 3 cellular phase, which is characterized by the infiltration of leukocytes to the site of injury [ ], and 4 resolution of inflammation, which is the process to return tissues to homeostasis [ , ].
In an infection by extracellular bacteria, the host triggers a series of responses to combat the pathogen and prevent its spread. The main mechanism of the innate immune response to eradicate bacteria is activation of the complement system, phagocytosis, and inflammatory response Figure 1.
Both the alternative and the lectin pathways of the complement system participate in the bacteria opsonization and potentiate their phagocytosis.
To perform the correct phagocytosis, activation of several surface receptors in phagocytes, including scavenger receptors, mannose, Fc, and mainly TLRs is required. Activation of these receptors results in inflammation, by recruiting leukocytes to the site of infection [ ].
On the other hand, the humoral adaptive immune response is the main protective against extracellular bacteria. Its primary function is to block infection, through the release of antibodies that are directed against the antigens of the bacterial cell wall, as well as of the toxins secreted by certain extracellular bacteria.
The effector mechanisms used by the antibodies include neutralization, opsonization, and classical complement pathway activation, which allow bacteria phagocytosis. The Th17 cells are also involved in recruiting monocytes and neutrophils, promoting local inflammation.
Immune response against bacteria. Mechanisms of the innate immune response to eradicate bacteria are A phagocytosis, B inflammatory response, and C participation of the complement system.
Description in the text. In the case of infection by intracellular bacteria, they have the ability to survive and replicate within phagocytic cells, which causes the circulating antibodies to be inaccessible to intracellular bacteria. The innate immune response against these bacteria is mediated primarily by phagocytes and NK cells [ ]. Among the phagocytes involved are neutrophils and then macrophages. However, these pathogens are resistant to degradation, but their products are recognized by TLRs and NLR receptors that are responsible for activating more phagocytes.
NK cells are also activated in this type of infections and participate by stimulating the production of cytokine IL by DCs and macrophages. But usually this immune response is ineffective against infection.
All this to eradicate the infection of the host [ ]. Most fungi are present in the environment, so animals including humans are exposed and then can inhale spores or yeasts [ ].
The mechanisms for defense against the fungi comprise of both innate and adaptive immune responses. TLR2 activation induces oxidative pathways in polymorphonuclear PMN cells with the release of gelatinases and inflammatory cytokines. TLRs can be combined to recognize a large number of fungal structures and thus generate a broader response against the various fungal structures [ , ]. Type C lectin receptors CTLRs make up a receptors family that can recognize several molecules like proteins, carbohydrates, and lipids.
Among these receptors, the best studied are dectin-1, dectin-2, dendritic cell-specific intercellular adhesion moleculegrabbing nonintegrin DC-SIGN , macrophage inducible C-type lectin, and mannose receptor MR involved in the recognition of some structures of the fungi [ ].
Dectin-1 activation can also induce mast cells to produce proinflammatory and TH2-polarizing cytokines, such as IL-4 and IL In addition, dectin-2 promotes Th17 polarization by inducing ILA, which is crucial in neutralizing some fungi.
The MR recognizes mannose, fucose, or N-acetylglucosamine residues present in fungi. MR generates a Th17 response and promotes fungi phagocytosis [ ]. The response that occurs through the activation of these receptors includes the binding to fungi and their phagocytosis, the induction of antifungal effector mechanisms and the production of soluble mediators such as cytokines, chemokines, and inflammatory lipids [ ].
The immunity against fungi requires the recruitment and activation of phagocytosis, which is mediated through factors that induce inflammatory molecules such as proinflammatory cytokines and chemokines.
The PRRs interaction with fungal structures plays an important role in the control of infections against these pathogens, since this interaction is determinant for the generation of the profile of cytokines or chemokines that influence the immune response.
Therefore, these interactions of the different fungal structures and the PRRs generate different responses polarizing toward one or the other depending on the cytokine profile that could be generated after these interactions Figure 2 [ ]. Immune response against fungi. The activation of these receptors includes the binding to fungi and their phagocytosis. In an infectious process, the most common host response is to generate inflammation.
Viruses in the absence of cytopathologic damage at early stages of infection inhibit the induction of acute phase protein response because early monocytes are not activated. Type I interferons are the major cytokines responsible for defending the human host against viral infections.
It has been shown that interferons do not exert their antiviral effects by direct action on viruses, but they help in the gene activation that results in the production of antiviral proteins, which participate as mediators in the inhibition of viral replication, as well as mediating the effects of suppressor T cells [ ]. The adaptive immune response against this type of infection is primarily composed of the humoral immune response with the antibody production directed against viral antigens.
However, the cellular immune response is the most important for virus eradication. Thus, both the innate immune response and the adaptive immune response in their cellular and humoral involvement eradicate viral infections in most cases Figure 3. However, certain viruses have developed mechanisms of immune evasion to survive longer and thus be able to replicate without any problem until causing serious damage to the host [ ]. Immune response against viruses. B Antibody production directed against viral antigens.
Due to there being a large variety of parasites and that each of their life cycles are very complex, in this section, we will focus on the immune response against helminth parasites.
This is because more than 1 billion people are currently infected with helminth parasites worldwide [ ], making them one of the most prevalent infectious agents responsible for many diseases in both animals and humans [ ]. The investigation of these parasitic infections is not only of direct relevance to human and animal health but also because they present a constant and important challenge to the host immune system, since both in humans and animals, helminth parasites establish chronic infections [ ] associated with a significant downregulation of the immune response.
Thus, helminth parasites will interact with the mucus layer and in many cases will have to cross it to reach the epithelial layer and thus thrive and reproduce within it [ ]. The immune response against helminth parasites involves both the innate and adaptive immune response [ , ]. Helminth parasite antigens are capable of inducing the DCs maturation, leading to the expression of MHC class II [ , ], promoting the development of a Th1 type cellular immune response Figure 4A [ ].
Immune response against parasites. Thanks to the authors who collaborated in the writing of this chapter: Dr. Pamela Castro, Dr. Alejandra Moreno and Dr.
Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3. Help us write another book on this subject and reach those readers. Login to your personal dashboard for more detailed statistics on your publications. Wozniak, B. Saunders, A. Ryan, and W. Roberts, J. Davies, G. Sempowski, and J. Feinen, A. Jerse, S. Gaffen, and M.
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