{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T04:29:09Z","timestamp":1791088149714,"version":"4.1.0"},"reference-count":25,"publisher":"Rockefeller University Press","issue":"12","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2002,12,16]]},"abstract":"<jats:p>CD4+ T cell help is important for the generation of CD8+ T cell responses. We used depleting anti-CD4 mAb to analyze the role of CD4+ T cells for memory CD8+ T cell responses after secondary infection of mice with the intracellular bacterium Listeria monocytogenes, or after boost immunization by specific peptide or DNA vaccination. Surprisingly, anti-CD4 mAb treatment during secondary CD8+ T cell responses markedly enlarged the population size of antigen-specific CD8+ T cells. After boost immunization with peptide or DNA, this effect was particularly profound, and antigen-specific CD8+ T cell populations were enlarged at least 10-fold. In terms of cytokine production and cytotoxicity, the enlarged CD8+ T cell population consisted of functional effector T cells. In depletion and transfer experiments, the suppressive function could be ascribed to CD4+CD25+ T cells. Our results demonstrate that CD4+ T cells control the CD8+ T cell response in two directions. Initially, they promote the generation of a CD8+ T cell responses and later they restrain the strength of the CD8+ T cell memory response. Down-modulation of CD8+ T cell responses during infection could prevent harmful consequences after eradication of the pathogen.<\/jats:p>","DOI":"10.1084\/jem.20011347","type":"journal-article","created":{"date-parts":[[2002,12,16]],"date-time":"2002-12-16T20:22:33Z","timestamp":1040070153000},"page":"1585-1592","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":167,"title":["Regulatory CD4+CD25+ T Cells Restrict Memory CD8+ T Cell Responses"],"prefix":"10.1084","volume":"196","author":[{"given":"Mischo","family":"Kursar","sequence":"first","affiliation":[{"name":"1Max Planck Institute for Infection Biology, Department of Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kerstin","family":"Bonhagen","sequence":"additional","affiliation":[{"name":"2Deutsches Rheumaforschungszentrum, Schumannstr. 21\/22, 10117 Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joachim","family":"Fensterle","sequence":"additional","affiliation":[{"name":"1Max Planck Institute for Infection Biology, Department of Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne","family":"Ko\u0308hler","sequence":"additional","affiliation":[{"name":"1Max Planck Institute for Infection Biology, Department of Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Hurwitz","sequence":"additional","affiliation":[{"name":"1Max Planck Institute for Infection Biology, Department of Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Kamradt","sequence":"additional","affiliation":[{"name":"2Deutsches Rheumaforschungszentrum, Schumannstr. 21\/22, 10117 Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan H.E.","family":"Kaufmann","sequence":"additional","affiliation":[{"name":"1Max Planck Institute for Infection Biology, Department of Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hans-Willi","family":"Mittru\u0308cker","sequence":"additional","affiliation":[{"name":"1Max Planck Institute for Infection Biology, Department of Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2002,12,9]]},"reference":[{"key":"2023072511370831000_BIB1","doi-asserted-by":"crossref","first-page":"129","DOI":"10.1146\/annurev.iy.11.040193.001021","volume":"11","year":"1993","journal-title":"Annu. 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