Malaria protection in beta 2-microglobulin-deficient mice lacking major histocompatibility complex class I antigens: essential role of innate immunity, including gammadelta T cells.
Immunology
; 122(4): 514-21, 2007 Dec.
Article
en En
| MEDLINE
| ID: mdl-17916163
ABSTRACT
It is still controversial whether malaria protection is mediated by conventional immunity associated with T and B cells or by innate immunity associated with extrathymic T cells and autoantibody-producing B cells. Given this situation, it is important to examine the mechanism of malaria protection in beta(2)-microglobulin-deficient (beta(2)m(-/-)) mice. These mice lack major histocompatibility complex class I and CD1d antigens, which results in the absence of CD8(+) T cells and natural killer T (NKT) cells. When C57BL/6 and beta(2)m(-/-) mice were injected with parasitized (Plasmodium yoelii 17XNL) erythrocytes, both survived from the infection and showed a similar level of parasitaemia. The major expanding T cells were NK1.1(-) alphabeta T-cell receptor(int) cells in both mice. The difference was a compensatory expansion of NK and gammadelta T cells in beta(2)m(-/-) mice, and an elimination experiment showed that these lymphocytes were critical for protection in these mice. These results suggest that malaria protection might be events of the innate immunity associated with multiple subsets with autoreactivity. CD8(+) T and NKT cells may be partially related to this protection.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Antígenos de Histocompatibilidad Clase I
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Subgrupos de Linfocitos T
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Microglobulina beta-2
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Receptores de Antígenos de Linfocitos T gamma-delta
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Malaria
Límite:
Animals
Idioma:
En
Revista:
Immunology
Año:
2007
Tipo del documento:
Article
País de afiliación:
Japón