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Chronic infection affects development of protective memory CD4 T cells in murine malaria
Author(s) -
Stephens Robin,
Langhorne Jean
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.22.1_supplement.858.7
Subject(s) - interleukin 7 receptor , plasmodium chabaudi , immunology , memory t cell , il 2 receptor , biology , t cell , phenotype , population , malaria , medicine , immune system , plasmodium falciparum , parasitemia , biochemistry , environmental health , gene
Both malaria infections and vaccines are reported to induce only short‐lived immunity; possibly due to lack of T cell memory, as both T cell cytokines and B cell help are critical. Using a T cell receptor transgenic mouse, where CD4 T cells recognize Plasmodium chabaudi, Merozoite Surface Protein‐1 (1157‐1171/I‐E d ); we investigated development of CD4 T cell memory and its part in protection against infection and pathology in chronic and drug‐treated infection. We observed that specific memory cells, as defined by surface phenotype (CD44 hi , CD25 − , IL7‐Rα hi , CD62L hi/lo ) and cytokine production (IFNγ hi , IL‐2 hi ) accumulated after one infection, and that although they were rapidly activated in a second infection, they did not proliferate faster than in a first infection. In a RAG transfer model, we observed that memory T cells from a drug‐limited infection allowed clearance of a challenge infection faster than naïve cells, but can increase pathology. Interestingly, chronic infection changed both memory phenotype and protective capacity of specific CD4 cells and maintained a memory population with a phenotype similar to effector cells (CD44 hi , IL7Rα − ) that protected no better than naïve CD4 T cells. (MRC)