Journal
JOURNAL OF IMMUNOLOGY
Volume 201, Issue 12, Pages 3569-3579Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1500497
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Funding
- National Institutes of Health (NIH)/National Institute of Arthritis and Musculoskeletal and Skin Diseases, Rheumatic Diseases Core Centers [P30AR053495-07]
- NIH/National Institute of Allergy and Infectious Disease [R01AI080850, R21AI101704]
- Canadian Institutes of Health Research
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R21AI101704, R01AI080850] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [P30AR053495] Funding Source: NIH RePORTER
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We examined the unique contributions of the cytokines IL-21 and IL-4 on germinal center (GC) B cell initiation and subsequent maturation in a murine model system. Similar to other reports, we found T follicular helper cell expression of IL-21 begins prior to T follicular helper cell migration into the B cell follicle and precedes that of IL-4. Consistent with this timing, IL-21 signaling has a greater influence on the perifollicular pre-GC B cell transition to the intrafollicular stage. Notably, Bcl6(hi) B cells can form in the combined absence of IL-21R- and STAT6-derived signals; however, these nascent GC B cells cease to proliferate and are more prone to apoptosis. When B cells lack either IL-21R or STAT6, aberrant GCs form atypical centroblasts and centrocytes that differ in their phenotypic maturation and costimulatory molecule expression. Thus, IL-4 and IL-21 play nonredundant roles in the phased progression of GC B cell development that can initiate in the combined absence of these cytokine signals.
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