B cells play a regulatory role in mice infected with the L3 of Brugia pahangi

• Published in: International immunology Vol. 17; no. 4; pp. 373 - 382
• Main Authors: Gillan, Victoria, Lawrence, Rachel A., Devaney, Eileen
• Format: Journal Article
• Language: English
• Published: England Oxford University Press 01.04.2005; Oxford Publishing Limited (England)
• Subjects: [3H]TdR [3H]thymidine; Animals; antigen presentation; Antigens, CD - immunology; APC antigen-presenting cells; B-Lymphocytes - immunology; B7-1 and B7-2; B7-1 Antigen - immunology; B7-2 Antigen; Brugia pahangi; Brugia pahangi - immunology; Cell Proliferation; CFSE carboxyfluorescein diacetate succinimidyl; co-stimulation; DC dendritic cells; DEPC diethyl pyrocarbonate; Filariasis - immunology; Flow Cytometry; IL-10; Interleukin-10 - metabolism; KLH keyhole limpet haemocyanin; L3 third stage larvae; Larva - immunology; Ligands; LNFPIII lacto-N-fucopentaose; Male; Membrane Glycoproteins - immunology; Mf microfilariae; Mice; Mice, Inbred BALB C; Nematoda; OVA ovalbumin peptide; p.i. post-infection; Receptors, Interleukin - antagonists & inhibitors; Receptors, Interleukin-10; RT reverse transcription; s.c. subcutaneously; Spleen - cytology; Spleen - immunology; Spleen - metabolism; WT wild-type
• ISSN: 0953-8178; 1460-2377
• DOI: 10.1093/intimm/dxh217

Mice infected with the L3 of the filarial nematode Brugia pahangi make a strong Th2 response characterized by elevated levels of antigen-specific IL-4, IL-5 and IL-10. Here we show that B cells from these animals are the major proliferating population in vitro with depletion of B cells or infection of μMT mice, resulting in reduced levels of antigen-specific proliferation. B cells also act as antigen-presenting cells (APC) to CD4+ cells as demonstrated by the switch in cytokine profiles upon B cell depletion. The efficiency of B cells in antigen presentation is attenuated by IL-10 which down-regulates the expression of B7-1 and B7-2 on the surface of B cells both in vitro and in vivo. Thus, IL-10 may modulate CD4 responses in L3-infected mice by suppressing the expression of B7 ligands on B cells. In support of this hypothesis, blockade of the IL-10R in vivo results in increased proliferation of CD4+ cells. We propose that B cells participate in a negative feedback loop: IL-10 elicited by infection with L3 and produced by B cells (and CD4+ cells) down-regulates the expression of B7 molecules on the B cell surface, attenuating their efficiency as APC to CD4+ T cells and restricting their expansion.