Class I HLA-restricted cytotoxic T lymphocyte responses against malaria-elucidation on the basis of HLA peptide binding motifs

Doolan, Denise L., Wizel, Benjamin, and Hoffman, Stephen L. (1996) Class I HLA-restricted cytotoxic T lymphocyte responses against malaria-elucidation on the basis of HLA peptide binding motifs. Immunologic Research, 15 (4). pp. 280-305.

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Abstract

In animal models, CD8+ T cells are a critical effector mechanism in the protective immunity against malaria. Conventional approaches to the development of many vaccines, including those against malaria, have however proved inadequate. In particular, an alternative approach is needed for the development of vaccines designed to induce a cellular immune response mediated by CD8+ T cells. Advances in the field of molecular immunology during the past decade have provided an insight into the presentation of peptides by MHC class I molecules and their recognition by CD8+ T cells. These studies have provided a conceptual basis for the development of efficacious parasitic and viral vaccines. By a combination of immunochemical and cellular immunologic analyses based on specific peptide binding motifs, a subunit malaria vaccine that includes CD8+ T cell epitopes restricted by the most common class I HLA alleles, including HLA-A2, can now be constructed.

Item ID: 42780
Item Type: Article (Refereed Research - C1)
Keywords: malaria, HLA-A2, cytotoxic T lymphocytes, HLA peptide binding motifs, HLA-restricted cytotoxic T lymphocytes
ISSN: 1559-0755
Funders: Naval Medical Research and Development Command (NMRDC), National Research Council, Naval Medical Research Institute
Projects and Grants: NMDRC Work Unit 63002A.00101-HFX, NMDRC Work Unit 6287A00101EFX.1432, NMDRC Work Unit 61102A.00101-BFX.1431
Date Deposited: 13 Sep 2016 03:25
FoR Codes: 11 MEDICAL AND HEALTH SCIENCES > 1107 Immunology > 110799 Immunology not elsewhere classified @ 100%
SEO Codes: 92 HEALTH > 9201 Clinical Health (Organs, Diseases and Abnormal Conditions) > 920109 Infectious Diseases @ 100%
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