{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T06:13:39Z","timestamp":1790144019869,"version":"4.0.1"},"reference-count":33,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2015,5,1]],"date-time":"2015-05-01T00:00:00Z","timestamp":1430438400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2015,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Anti-CD20 antibody therapy has been a useful medication for managing non-Hodgkin's lymphoma as well as autoimmune diseases characterized by autoantibody generation. CD20 is expressed during most developmental stages of B lymphocytes; thus, CD20 depletion leads to B-lymphocyte deficiency. As the drug has become more widely used, there has been an increase in the number of case reports of patients developing\n            <jats:named-content content-type=\"genus-species\">Pneumocystis<\/jats:named-content>\n            pneumonia. The role of anti-CD20 in\n            <jats:named-content content-type=\"genus-species\">Pneumocystis jirovecii<\/jats:named-content>\n            infection is under debate due to the fact that most patients receiving it are on a regimen of multiple immunosuppressive medications. To address the specific role of CD20 depletion in host immunity against\n            <jats:named-content content-type=\"genus-species\">Pneumocystis<\/jats:named-content>\n            , we examined a murine anti-CD20 depleting antibody. We demonstrated that anti-CD20 alone is permissive for\n            <jats:named-content content-type=\"genus-species\">Pneumocystis<\/jats:named-content>\n            infection and that anti-CD20 impairs components of type II immunity, such as production of interleukin-4 (IL-4), IL-5, and IL-13 by whole-lung cells, in response to\n            <jats:named-content content-type=\"genus-species\">Pneumocystis murina<\/jats:named-content>\n            . We also demonstrated that CD4\n            <jats:sup>+<\/jats:sup>\n            T cells from mice treated with anti-CD20 during\n            <jats:named-content content-type=\"genus-species\">Pneumocystis<\/jats:named-content>\n            infection are incapable of mounting a protective immune response when transferred into Rag1\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice. Thus, CD20\n            <jats:sup>+<\/jats:sup>\n            cells are critical for generating protective CD4\n            <jats:sup>+<\/jats:sup>\n            T-cell immune responses against this organism.\n          <\/jats:p>","DOI":"10.1128\/iai.03099-14","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T03:13:25Z","timestamp":1425352405000},"page":"2043-2052","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":63,"title":["Anti-CD20 Antibody Therapy and Susceptibility to Pneumocystis Pneumonia"],"prefix":"10.1128","volume":"83","author":[{"given":"Waleed","family":"Elsegeiny","sequence":"first","affiliation":[{"name":"Department of Immunology, University of Pittsburgh School of Medicine (UPSOM), Pittsburgh, Pennsylvania, USA"},{"name":"Richard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania, 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