CD8-suppressor factor and β-chemokine function as a complementary mechanism to cognate immunity

• Published in: Immunology letters 1999-03, Vol.66 (1), p.171-176
• Main Authors: Lehner, Thomas, Wang, Yufei, Tao, Louisa, Bergmeier, LesleyA, Mitchell, Elaine, Doyle, Carl
• Format: Article
• Language: English
• Subjects: AIDS/HIV; Animals; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes - immunology; CD8-suppressor factor; Chemokines, CC - immunology; Gene Products, gag - immunology; HIV Envelope Protein gp120 - immunology; Humans; Lymph Nodes - immunology; Macaca mulatta; Male; Membrane Glycoproteins; Recombinant Proteins - immunology; SIV; Suppressor Factors, Immunologic - immunology; Targeted immunisation; Vaccination; Viral Envelope Proteins; Virus Replication; Xenoimmunisation; β-chemokines
• ISSN: 0165-2478; 1879-0542
• DOI: 10.1016/S0165-2478(98)00155-2

Protection against SIV or HIV infection requires specific antibodies and T-cell immune responses. However, a complementary mechanism may be involved, in which CD8-suppressor factors (CD8-SF) and the constitutive β-chemokines may prevent the virus binding and replicating. Indeed, there is evidence that targeted iliac lymph node (TILN) immunisation with SIVgp120 and p27 or xenoimmunisation with SIV grown in human T-cells generates CD8-SF, RANTES, MIP-1α and MIP-1β which are significantly correlated with protection from SIV infection by the rectal mucosal or intravenous route, respectively. Inhibition of SIV replication in vitro is dependent on the concentration of β-chemokines generated by immunisation. The critical level for inhibition of SIV replication appears to be higher for rectal mucosal than intravenous challenge by SIV. The mechanism of protection in vivo has not been elucidated but it is likely that the β-chemokines bind to CCR5 coreceptors which are internalised. Thus, CCR5 coreceptors are either blocked or not expressed on the cell surface for SIV to bind and infect.