Premium
Differential responses to cyclosporine A in a delayed type hypersensitivity model
Author(s) -
MacLeod Heather D.,
Goodwin Debbie,
Damphousse Christy,
NickersonNutter Cheryl
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.387
Subject(s) - immunology , inflammation , lymph , cytokine , antigen , t cell , adjuvant , delayed hypersensitivity , medicine , immune system , pathology
DTH is classically defined as a model of inflammation involving antigen presentation, T cell activation and cytokine production. Understanding the etiology of the reaction is important, as DTH is commonly used to assess the efficacy of reagents targeting pathways involved in inflammation. We studied the sRBC induced DTH response in two different mouse strains, the commonly used Balb/c and autoimmune prone B6D2F1. Both mouse strains exhibited equivalent paw swelling, but interestingly, CsA treatment reduced swelling in Balb/c but not in B6D2F1 mice. Restimulation of T cells from the draining lymph nodes demonstrates that Balb/c T cells produce greater levels of IFNγ, TNFα and IL‐10 compared to B6D2F1 T cells, suggesting that Balb/c DTH may be more cytokine mediated than B6D2F1 DTH. Moreover, IFNγ deficient mice on the Balb/c background have reduced DTH. Although the development of autoantibodies in B6D2F1 mice has been linked to IL‐17, we found that treatment with αIL‐17A or αIL‐17F had no effect on DTH in either strain. Our results indicate that the pathology of the DTH response is different in Balb/c compared to B6D2F1 mice, implying that different etiologies are involved. Therefore, understanding the DTH response in a particular strain of mouse is important in order to accurately determine the specific pathways responsible for the resultant inflammation.