Induction of macrophage motility by a T-cell line from Balb/c mice specific for Plasmodium berghei malaria.
A long-term antimalaria T-cell line (AMTL) expressing a helper phenotype (Thy 1.2+, Lyt 2.2-) was established from Plasmodium berghei-recovered Balb/c mice. The ability of this T-line to induce macrophage motility was measured in vivo and in vitro. Adoptive transfer of AMTL cells to normal Balb/c mice showed an increased delayed hypersensitivity response to the homologous antigen, i.e., parasitized erythrocytes (PE). In vitro, AMTL culture supernatant (AMTL-SUP) augmented chemotactic locomotion of macrophages derived from both normal and infected mice. However, the effect on normal macrophages was significantly higher. AMTL cells adoptively transferred to normal mice had no effect on parasitemia levels or mortality rate after subsequent infection with P. berghei. Partial characterization of the AMTL-SUP indicated the involvement of a protein of about 12,600 Daltons in the enhancement of chemotaxis. These findings suggest that the AMTL cells and chemoattractants produced by them can induce macrophage motility, and that the macrophage malfunction in Balb/c with P. berghei infection is not due to defects at the T-lymphocyte level.
Gross
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Department of Parasitology, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Frankenburg
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D000818:Animals; D002460:Cell Line; D002630:Chemotactic Factors / Q000502:physiology*; D002633:Chemotaxis; D005260:Female; D006358:Hot Temperature; D006968:Hypersensitivity, Delayed; D008264:Macrophages / Q000276:immunology* / Q000502:physiology; D008288:Malaria / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008970:Molecular Weight; D010447:Peptide Hydrolases / Q000378:metabolism; D010962:Plasmodium berghei; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*
D002630:Chemotactic Factors; D010447:Peptide Hydrolases