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Antibodies attack IL-17.

Maxmen A - J. Exp. Med. (2010)

View Article: PubMed Central - HTML - PubMed

Affiliation: amaxmen@rockefeller.edu

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According to Puel et al. and Kisand et al., APS-I patients produce autoantibodies against microbe-fighting cytokines—making this disorder one of a small handful of diseases enhanced by antibodies that target cytokines... The yeast infection, known as chronic mucocutaneous candidiasis, usually develops before other symptoms of APS-I... The infection is perplexing given that many autoimmune disorders are characterized by exaggerated Th17 cell responses, which produce cytokines like interleukin (IL)-17A, IL-17F, and IL-22 that fight microbial pathogens at mucosal surfaces... On the contrary, here the teams suggest that APS-I patients have diminished Th17 activity due to autoantibodies against these signature cytokines... Kisand et al. found that cultured progenitor cells from APS-I patients produced less IL-17F and IL-22 in response to yeast antigens or polyclonal stimuli... And although some cells made less IL-17A as well, cytokine levels varied overall, likely reflecting variation in genetic, environmental, or clinical backgrounds... The paucity of cytokines correlated with the presence of autoantibodies against IL-17A, IL-17F, and IL-22... These autoantibodies blocked or neutralized the cytokines but, according to Kisand et al., did not obstruct Th17 cell differentiation... Other inflammatory cytokines were unaffected, with the exception of interferon (IFN)-ɑ, which is known to be blocked by autoantibodies in APS-I patients... However, APS-I patients do not appear prone to recurrent viral infections despite neutralization of this antiviral cytokine—perhaps because other IFNs compensate.

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APS-I patients harbored autoantibodies against IFN-α, IL-17A, IL-17F, and IL-22.
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fig1: APS-I patients harbored autoantibodies against IFN-α, IL-17A, IL-17F, and IL-22.


Antibodies attack IL-17.

Maxmen A - J. Exp. Med. (2010)

APS-I patients harbored autoantibodies against IFN-α, IL-17A, IL-17F, and IL-22.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2822608&req=5

fig1: APS-I patients harbored autoantibodies against IFN-α, IL-17A, IL-17F, and IL-22.

View Article: PubMed Central - HTML - PubMed

Affiliation: amaxmen@rockefeller.edu

AUTOMATICALLY GENERATED EXCERPT
Please rate it.

According to Puel et al. and Kisand et al., APS-I patients produce autoantibodies against microbe-fighting cytokines—making this disorder one of a small handful of diseases enhanced by antibodies that target cytokines... The yeast infection, known as chronic mucocutaneous candidiasis, usually develops before other symptoms of APS-I... The infection is perplexing given that many autoimmune disorders are characterized by exaggerated Th17 cell responses, which produce cytokines like interleukin (IL)-17A, IL-17F, and IL-22 that fight microbial pathogens at mucosal surfaces... On the contrary, here the teams suggest that APS-I patients have diminished Th17 activity due to autoantibodies against these signature cytokines... Kisand et al. found that cultured progenitor cells from APS-I patients produced less IL-17F and IL-22 in response to yeast antigens or polyclonal stimuli... And although some cells made less IL-17A as well, cytokine levels varied overall, likely reflecting variation in genetic, environmental, or clinical backgrounds... The paucity of cytokines correlated with the presence of autoantibodies against IL-17A, IL-17F, and IL-22... These autoantibodies blocked or neutralized the cytokines but, according to Kisand et al., did not obstruct Th17 cell differentiation... Other inflammatory cytokines were unaffected, with the exception of interferon (IFN)-ɑ, which is known to be blocked by autoantibodies in APS-I patients... However, APS-I patients do not appear prone to recurrent viral infections despite neutralization of this antiviral cytokine—perhaps because other IFNs compensate.

Show MeSH
Related in: MedlinePlus