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Promotion of a functional B cell germinal center response after Leishmania species co-infection is associated with lesion resolution
Journal article   Open access   Peer reviewed

Promotion of a functional B cell germinal center response after Leishmania species co-infection is associated with lesion resolution

Katherine N Gibson-Corley, Paola M Boggiatto, Marie M Bockenstedt, Christine A Petersen, Thomas J Waldschmidt and Douglas E Jones
The American journal of pathology, Vol.180(5), pp.2009-2017
05/2012
DOI: 10.1016/j.ajpath.2012.01.012
PMCID: PMC3349825
PMID: 22429963
url
https://doi.org/10.1016/j.ajpath.2012.01.012View
Published (Version of record) Open Access

Abstract

Co-infection of C3HeB/FeJ (C3H) mice with both Leishmania major and Leishmania amazonensis leads to a healed footpad lesion, whereas co-infection of C57BL/6 (B6) mice leads to non-healing lesions. This inability to heal corresponds to a deficiency in B cell stimulation of the macrophage-mediated killing of L. amazonensis in vitro and a less robust antibody response. The mechanism that leads to healing of these lesions is not completely known, although our studies implicate the B cell response as having an important effector function in killing L. amazonensis. To understand more completely this disparate clinical outcome to the same infection, we analyzed the draining lymph node germinal center B cell response between co-infected C3H and B6 mice. There were more germinal center B cells, more antibody isotype-switched germinal center B cells, more memory B cells, and more antigen-specific antibody-producing cells in co-infected C3H mice compared to B6 mice as early as 2 weeks postinfection. Interleukin (IL)-21 production and IL-21 receptor expression in both mouse strains, however, were similar at 2 weeks, suggesting that the difference in the anti-Leishmania response in these mouse strains may be due to differences in T follicular cell commitment or intrinsic B cell differences. These data support the idea that functional B cells are important for healing L. amazonensis in this infectious disease model.
Leishmania major - immunology Antigens, Protozoan - immunology Prognosis Species Specificity Coinfection - immunology Germinal Center - immunology Mice, Inbred C57BL Immunoglobulin Class Switching - immunology Receptors, Interleukin-21 - metabolism Lymph Nodes - immunology Leishmaniasis, Cutaneous - immunology Mice, Inbred C3H Antibodies, Protozoan - biosynthesis Animals B-Lymphocytes - immunology Immunoglobulin G - biosynthesis Leishmaniasis, Cutaneous - parasitology Female Immunologic Memory Mice Interleukins - biosynthesis Leishmania mexicana - immunology

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