Kelly A. Hagadorn, Mary E. Peterson, Hemanta Kole, Bethany Scott, Jeff Skinner, Ababacar Diouf, Eizo Takashima, Aissata Ongoiba, Safiatou Doumbo, Didier Doumtabe, Shanping Li, Padmapriya Sekar, Mei Yan, Chengsong Zhu, Hikaru Nagaoka, Bernard N. Kanoi, Quan-Zhen Li, Carole Long, Eric O. Long, Kassoum Kayentao, Christine S. Hopp
{"title":"Autoantibodies inhibit Plasmodium falciparum growth and are associated with protection from clinical malaria","authors":"Kelly A. Hagadorn, Mary E. Peterson, Hemanta Kole, Bethany Scott, Jeff Skinner, Ababacar Diouf, Eizo Takashima, Aissata Ongoiba, Safiatou Doumbo, Didier Doumtabe, Shanping Li, Padmapriya Sekar, Mei Yan, Chengsong Zhu, Hikaru Nagaoka, Bernard N. Kanoi, Quan-Zhen Li, Carole Long, Eric O. Long, Kassoum Kayentao, Christine S. Hopp","doi":"10.1016/j.immuni.2024.05.024","DOIUrl":null,"url":null,"abstract":"<p>Many infections, including malaria, are associated with an increase in autoantibodies (AAbs). Prior studies have reported an association between genetic markers of susceptibility to autoimmune disease and resistance to malaria, but the underlying mechanisms are unclear. Here, we performed a longitudinal study of children and adults (<em>n</em> = 602) in Mali and found that high levels of plasma AAbs before the malaria season independently predicted a reduced risk of clinical malaria in children during the ensuing malaria season. Baseline AAb seroprevalence increased with age and asymptomatic <em>Plasmodium falciparum</em> infection. We found that AAbs purified from the plasma of protected individuals inhibit the growth of blood-stage parasites and bind <em>P. falciparum</em> proteins that mediate parasite invasion. Protected individuals had higher plasma immunoglobulin G (IgG) reactivity against 33 of the 123 antigens assessed in an autoantigen microarray. This study provides evidence in support of the hypothesis that a propensity toward autoimmunity offers a survival advantage against malaria.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":null,"pages":null},"PeriodicalIF":25.5000,"publicationDate":"2024-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Immunity","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.immuni.2024.05.024","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Many infections, including malaria, are associated with an increase in autoantibodies (AAbs). Prior studies have reported an association between genetic markers of susceptibility to autoimmune disease and resistance to malaria, but the underlying mechanisms are unclear. Here, we performed a longitudinal study of children and adults (n = 602) in Mali and found that high levels of plasma AAbs before the malaria season independently predicted a reduced risk of clinical malaria in children during the ensuing malaria season. Baseline AAb seroprevalence increased with age and asymptomatic Plasmodium falciparum infection. We found that AAbs purified from the plasma of protected individuals inhibit the growth of blood-stage parasites and bind P. falciparum proteins that mediate parasite invasion. Protected individuals had higher plasma immunoglobulin G (IgG) reactivity against 33 of the 123 antigens assessed in an autoantigen microarray. This study provides evidence in support of the hypothesis that a propensity toward autoimmunity offers a survival advantage against malaria.
期刊介绍:
Immunity is a publication that focuses on publishing significant advancements in research related to immunology. We encourage the submission of studies that offer groundbreaking immunological discoveries, whether at the molecular, cellular, or whole organism level. Topics of interest encompass a wide range, such as cancer, infectious diseases, neuroimmunology, autoimmune diseases, allergies, mucosal immunity, metabolic diseases, and homeostasis.