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Chapter 10 : Microbial Superantigens and Immunological Deregulation

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Abstract:

Superantigens are usually regarded as potent inducers of an overwhelming (unmodulated) immune response that manifests as a rare event, such as toxic shock syndrome or food poisoning. This chapter presents evidence that immune response to superantigens may well trigger or exacerbate autoimmunity. Multiple sclerosis (MS) symptomology can often be observed to occur in a relapsing-remitting manner. Superantigen effects are suggested by studies of peripheral and synovial Vβ14 T cells from patients with rheumatoid arthritis versus those from controls and of B-cell production of rheumatoid factor upon stimulation with SED. Skin lesion eruptions in guttate psoriasis have been linked with throat infections and increased antibody titers to streptococcal antigens. Initial studies of the infectivity of mouse mammary tumor virus (MMTV) indicated that an intact immune system was required for infection. Antibodies to IL-10 block the protective effects of IL-10 against experimental allergic encephalomyelitis (EAE). Focusing on cell cycle events, the authors have determined the effects of IL-10 on the entry of quiescent CD4 T cells into the cell cycle upon stimulation with the staphylococcal superantigen staphylococcal enterotoxin B (SEB). The long-term effects of superantigen activation of T cells can include the induction of autoreactive cells, leading to an autoimmune state. Superantigens can also cause relapses into disease in patients with remission.

Citation: Torres B, Perrin G, Johnson H, Soos J. 2000. Microbial Superantigens and Immunological Deregulation, p 183-197. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch10

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Immune Systems
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Toxic Shock Syndrome Toxin 1
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Major Histocompatibility Complex
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FIGURE 1

Differences between conventional antigens and superantigens.

Citation: Torres B, Perrin G, Johnson H, Soos J. 2000. Microbial Superantigens and Immunological Deregulation, p 183-197. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch10
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FIGURE 2

Modulation of EAE by superantigens with different Vβ specificities. The predicted outcome of the hypothesis proposed is denoted by “EAE” (induction of disease) and “No EAE” (absence of disease). The predicted outcome was confirmed by studies of the development of EAE after administration of either SEA or SEB. (A) In the first group, SEB pretreatment prevented development of EAE following injection of MBP, and while mice administered a second dose of SEB were refractory to development of disease, mice administered SEA exhibited accelerated onset of EAE. (B) In the second group, SEA pretreatment did not prevent EAE. After resolution o f clinical symptoms, administration o f a second dose o f SEA did not reactivate disease. SEB administration, however, did reactivate EAE in the SEA-pretreated mice.

Citation: Torres B, Perrin G, Johnson H, Soos J. 2000. Microbial Superantigens and Immunological Deregulation, p 183-197. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch10
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FIGURE 3

Model for t h e role of N e f in the pathogenesis of HIV. Soluble N e f released by lysed infected cells binds to H L A - D R o n antigen-presenting cells or is an integral component of the cell membranes of infected T cells. N e f is then presented to uninfected T cells, causing proliferation and activation o f T cells with concomitant cytokine production. Such proliferation results in a cellular reservoir for virus replication. Differentiation of B cells may possibly b e mediated by release of T-cell cytokines.

Citation: Torres B, Perrin G, Johnson H, Soos J. 2000. Microbial Superantigens and Immunological Deregulation, p 183-197. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch10
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FIGURE 4

Antitumor responses in the absence and presence of superantigens. Limited antitumor responses are elicited by poorly immunogenic tumors even after vaccination with inactivated tumor cells. However, administration of superantigens after vaccination with inactivated tumor cells stimulates amplified antitumor responses, augmenting specific antitumor immunity.

Citation: Torres B, Perrin G, Johnson H, Soos J. 2000. Microbial Superantigens and Immunological Deregulation, p 183-197. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch10
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Tables

Generic image for table
TABLE 1

Human diseases associated with bacterial and viral superantigens

Citation: Torres B, Perrin G, Johnson H, Soos J. 2000. Microbial Superantigens and Immunological Deregulation, p 183-197. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch10
Generic image for table
TABLE 2

Effect of staphylococcal superantigens on B16F10 melanoma tumor growth

Citation: Torres B, Perrin G, Johnson H, Soos J. 2000. Microbial Superantigens and Immunological Deregulation, p 183-197. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch10

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