An Optimized CD4 T-Cell Response Can Control Productive and Latent Gammaherpesvirus Infection

Abstract

CD4 T cells are important for control of infection with murine gammaherpesvirus 68 (␥HV68),

Murine gammaherpesvirus 68 infection protects lupus-prone mice from the development of autoimmunity

“…This chronic infection persists for the rest of the individual's life. Reactivation of the virus can periodically occur, but this is regulated by the host immune system (13,15,(22)(23)(24)(25)(26)(27)(28).…”

“…This chronic infection persists for the rest of the individual's life. Reactivation of the virus can periodically occur, but this is regulated by the host immune system (13,15,(22)(23)(24)(25)(26)(27)(28).A previous study has shown that γHV68 infection of WT C57BL/6 (B6) mice promotes expression of dsDNA and collagen-reactive IgG autoantibodies (12). These autoantibodies, moreover, persisted as long as 80 d after infection, after the time the virus has entered its latent phase.…”

Adoptive transfer of cytomegalovirus‐specific effector CD4+T cells provides antiviral protection from murine CMV infection

“…Despite the prominent roles of cytotoxic CD8 + T cells and neutralizing antibodies in controlling viral infections, there is growing evidence for an antiviral role of CD4 + helper T cells, not only in provision of help to other effector cells, but also in exertion of direct antiviral functions either by secretion of cytokines or exertion of cytotoxicity [1]. CD4 + T-cell-mediated protective immunity has been reported Correspondence: Prof. Annette Oxenius e-mail: oxenius@micro.biol.ethz.ch for a number of viral infections [2][3][4][5]; however, the antiviral effector mechanisms exerted by CD4 + T cells in vivo have remained poorly characterized.Cytomegalovirus (CMV) is a β-herpes virus that infects a majority of the human population worldwide. After resolution of primary infection, this large DNA β-herpes virus establishes a life-long persistence in its host.…”

Immune surveillance of intracellular pathogens via autophagy

“…Thus, autophagic degradation contributes to MHC class II presentation of intracellular antigens to CD4 þ T cells cytotoxic effects on virus-infected cells [85][86][87][88] and contribute to the control of viral infections. [89][90][91][92][93] Given these important roles of CD4 þ T cells for adaptive immunity, it seems crucial that endogenous antigen be presented not only on MHC class I, but also on MHC class II. We suggest that part of these endogenous MHC class II ligands are generated from autophagy substrates and that MHC class II presentation of long-lived endogenous substrates complements MHC class I presentation of short-lived endogenous substrates to elicit T-cell activation during immune responses.…”