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Role of CD8+ T lymphocytes in the genesis of angiotensin II‐induced hypertension
Author(s) -
Thabet Salim Riad,
Chen Wei,
Harrison David
Publication year - 2010
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.24.1_supplement.lb564
Subject(s) - cd8 , adoptive cell transfer , angiotensin ii , endocrinology , medicine , inflammation , cytotoxic t cell , t lymphocyte , infiltration (hvac) , blood pressure , immunology , biology , t cell , immune system , in vitro , biochemistry , physics , thermodynamics
We have shown previously that T lymphocytes play a major role in the genesis of both angiotensin II‐induced and DOCA‐salt hypertension. T cells include CD4+ helper cells and CD8+ cells, but the role of these subsets in hypertension is unclear. Mice lacking CD8+ lymphocytes (CD8 −/− ) exhibited a markedly blunted hypertensive response to angiotensin II (SBP: 132 ± 8 mmHg), while CD4 −/− mice had a normal hypertensive response to this octapeptide (SBP: 178 ± 6 mmHg). Consistent with this, adoptive transfer of CD8+ from hypertensive mice to RAG1 −/− caused a significant rise in blood pressure in the recipients, while transfer of CD4+ cells did not (SBPs: 188 ± 4 mmHg vs. 144 ± 6 mmHg respectively). In C57Bl/6 mice, angiotensin II stimulates marked infiltration of leukocytes and T cells into the perivascular fat, and this was markedly reduced in CD8 −/− mice. We also found that hypertension increases IFNγ and TNFα production by CD8+ cells. These studies identify a previously undefined role for CD8+ cells in the genesis of hypertension and its attendant inflammation. Future studies are needed to elucidate the mechanisms of CD8+ cell involvement in this disease.