In:
Infection and Immunity, American Society for Microbiology, Vol. 74, No. 5 ( 2006-05), p. 2717-2725
Abstract:
Little is known about the function and regulation of splenic γδ T cells during chronic Plasmodium chabaudi malaria. The splenic γδ T-cell population continues to expand, reaching levels equal to 4 times the number of splenocytes in an uninfected mouse. Splenic γδ T cells from J H −/− mice with chronic malaria expressed Vγ1 + or Vδ4 + in the same ratio as uninfected controls with Vγ1 cells dominating, but the Vγ2 ratio declined about twofold. γδ T cells from G8 mice specific for the TL antigen increased only 2-fold in number, compared with 10-fold in BALB/c controls, but G8 γδ T cells failed to express the B220 activation marker. Elimination of the parasite by drug treatment caused a slow depletion in the number of splenic γδ, CD4 + , and CD8 + T cells. Following challenge, drug-cured J H −/− mice exhibited nearly identical parasitemia time courses as naïve controls. Depletion of either CD4 + T cells or γδ T cells from chronically infected J H −/− mice by monoclonal antibody treatment resulted in an immediate and significant ( P 〈 0.05) exacerbation of parasitemia coupled with a marked decrease in splenic γδ T-cell numbers. The number of CD4 + T cells, in contrast, did not decrease in mice after anti-T-cell receptor γδ treatment. The results indicate that cell-mediated immunity against blood-stage malarial parasites during chronic malaria (i) requires the continued presence of blood-stage parasites to remain functional, (ii) is dependent upon both γδ T cells and CD4 + T cells, and (iii) lacks immunological memory.
Type of Medium:
Online Resource
ISSN:
0019-9567
,
1098-5522
DOI:
10.1128/IAI.74.5.2717-2725.2006
Language:
English
Publisher:
American Society for Microbiology
Publication Date:
2006
detail.hit.zdb_id:
1483247-1
