Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 1, Pages 230-237Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.1.230
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Funding
- NCI NIH HHS [CA13148] Funding Source: Medline
- NIAID NIH HHS [R01 AI014782, AI14782] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P30CA013148] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI014782, R21AI014782] Funding Source: NIH RePORTER
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Of a number of mAbs made by immunization with sort-purified marginal zone (MZ) B cells, one was shown to recognize the mouse scavenger receptor CD36. Although CD36 is expressed by most resting MZ B cells and not by follicular and B1 B cells, it is rapidly induced on follicular B cells in vitro following TLR and CD40 stimulation. In response to T-independent and T-dependent Ag challenge, we found that CD36 was expressed on IgM(+) plasma cells, but down-regulated on isotype-switched plasma cells in vivo. Although development, localization, and phenotype of MZ B cells in CD36(-/-) mice appeared normal, there was a minor block in the transitional stages of mature B cell development. In both primary and secondary Ab responses to heat-killed Streptococcus pneumoniae (R36A strain), both phosphoryl choline (PC)-specific IgM and IgG levels in CD36(-/-) mice were slightly reduced compared with Nvild-type mice. In addition, mice deficient in both TLR2 and CD36 produced significantly reduced levels of anti-PC IgG titers than those of single gene-deficient mice, suggesting that they may cooperate in an anti-PC Ab response. Collectively, these results show that CD36 does not affect the development of B cells, but modulates both primary and secondary anti-PC Ab responses during S. pneumoniae infection similarly to TLR2.
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