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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 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... 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... How these autoantibodies arise remains a mystery... The authors suggest that their origin may be due to mutations in the gene underlying APS-I, which disrupt the autoimmune regulator AIRE... AIRE normally prevents autoreactive T cells from leaving the thymus, but a direct connection between the AIRE disruption and anti-cytokine antibodies remains to be seen.

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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 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... 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... How these autoantibodies arise remains a mystery... The authors suggest that their origin may be due to mutations in the gene underlying APS-I, which disrupt the autoimmune regulator AIRE... AIRE normally prevents autoreactive T cells from leaving the thymus, but a direct connection between the AIRE disruption and anti-cytokine antibodies remains to be seen.

Show MeSH
Related in: MedlinePlus