Residual LCMV antigen in transiently CD4 T cell-depleted mice induces high levels of virus-specific antibodies but only limited B-cell memory.

Infection of C57BL/6 mice with lymphocytic choriomeningitis virus (LCMV) strain Armstrong (Arm) induces an acute infection with rapid virus clearance by CD8 T cells independently of CD4 T cell help. Residual viral antigen may, however, persist for a prolonged time. Here, we demonstrate that mice that had been transiently depleted of CD4 T cells during acute LCMV Arm infection generated high levels of virus-specific IgG antibodies (Ab) after viral clearance.

Immunological tolerance to LCMV antigens differently affects control of acute and chronic virus infection in mice.

Cytotoxic T lymphocytes (CTLs) play a key role in the control of lymphocytic choriomeningitis virus (LCMV) infection. In C57BL/6 mice (H-2 ), the CTL response is mainly directed against epitopes from the LCMV glycoprotein (GP) and the nucleoprotein (NP) which represent the two major viral proteins. The role of GP- versus NP-derived epitopes for viral clearance was examined using transgenic (tg) mice ubiquitously expressing LCMV GP and NP, respectively.

KLRG1 activity is regulated by association with the transferrin receptor.

The killer cell lectin-like receptor G1 (KLRG1) is a cadherin-binding inhibitory receptor expressed by NK cells and differentiated T cells. Here, we surprisingly found that a fraction of KLRG1 molecules expressed in the murine A5 T-cell line and in IL-2-activated NK cells forms disulfide-linked heteromers with the transferrin receptor (TfR). Fluorescence microscopy additionally revealed substantial colocalization of KLRG1 and TfR in intracellular compartments and on the cell surface.

Nucleoprotein-specific nonneutralizing antibodies speed up LCMV elimination independently of complement and FcγR.

CD8(+) T cells have an essential role in controlling lymphocytic choriomeningitis virus (LCMV) infection in mice. Here, we examined the contribution of humoral immunity, including nonneutralizing antibodies (Abs), in this infection induced by low virus inoculation doses. Mice with impaired humoral immunity readily terminated infection with the slowly replicating LCMV strain Armstrong but showed delayed virus elimination after inoculation with the faster replicating LCMV strain WE and failed to clear the rapidly replicating LCMV strain Docile, which is in contrast to the results obtained with wild-type mice.

Different inhibitory capacities of human and mouse KLRG1 are linked to distinct disulfide-mediated oligomerizations.

The killer cell lectin-like receptor G1 (KLRG1) is a cadherin-binding inhibitory receptor expressed by NK and T cells in humans and mice. Although structural and ligand-binding properties of human (h) and mouse (m) KLRG1 are very similar, KLRG1-mediated inhibition under physiological conditions is only observed with human lymphocytes. Using a well-defined in vitro system, we demonstrate here that mKLRG1 exhibits a significantly lower inhibitory capacity compared with the human homolog.