Gamma delta T-cell function in pathogenesis of cerebral malaria in mice infected with Plasmodium berghei ANKA

• Published in: Infection and immunity Vol. 67; no. 1; pp. 446 - 448
• Main Authors: Yañez, D M, Batchelder, J, van der Heyde, H C, Manning, D D, Weidanz, W P
• Format: Journal Article
• Language: English
• Published: United States 01.01.1999
• Subjects: Animals; Antibodies, Monoclonal - administration & dosage; CD4-Positive T-Lymphocytes - immunology; CD8-Positive T-Lymphocytes - immunology; Disease Models, Animal; Female; Lymphocyte Depletion; Malaria, Cerebral - etiology; Malaria, Cerebral - immunology; Malaria, Cerebral - mortality; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Plasmodium berghei; Plasmodium berghei - immunology; Receptors, Antigen, T-Cell, gamma-delta - deficiency; Receptors, Antigen, T-Cell, gamma-delta - genetics; Receptors, Antigen, T-Cell, gamma-delta - immunology; T-Lymphocyte Subsets - immunology; T-Lymphocyte Subsets - metabolism
• ISSN: 0019-9567

Mice depleted of gammadelta T cells by monoclonal antibody treatment and infected with Plasmodium berghei ANKA did not develop cerebral malaria (CM). In striking contrast, delta0/0 mice infected with P. berghei developed CM despite their gammadelta T-cell deficiency. gammadelta T cells appear to be essential for the pathogenesis of CM in mice having experienced normal ontogeny but not in mice genetically deprived of gammadelta T cells from the beginning of life.