Inducible nitric oxide synthase is crucial for plasma cell survival.

The viability of long-lived plasma cells is enhanced by the expression of inducible nitric oxide synthase, which relieves endoplasmic reticulum stress by triggering a response dependent on cGMP and protein kinase G.

The CD28/B7 pathway: a novel regulator of plasma cell function.

The CD28/B7 pathway is pivotal for the activation, optimal function, and regulation of T cell function. While the CD28 receptor and its ligands B7.1/B7.

The enigma of memory B cells in malaria.

Malaria is a major public health problem particularly in the tropics. It is caused by protozoan parasites belonging to the genus Plasmodium and is transmitted by Anopheles mosquitoes. Currently, strategies to control malaria include vector control measures, chemoprophylaxis, and efficient diagnosis and treatment.

CD28-B7 interaction modulates short- and long-lived plasma cell function.

The interaction of CD28, which is constitutively expressed on T cells, with B7.1/B7.2 expressed on APCs is critical for T cell activation.

Costimulation modulation uncouples protection from immunopathology in memory T cell responses to influenza virus.

The rapid effector functions and tissue heterogeneity of memory T cells facilitate protective immunity, but they can also promote immunopathology in antiviral immunity, autoimmunity, and transplantation. Modulation of memory T cells is a promising but not yet achieved strategy for inhibiting these deleterious effects. Using an influenza infection model, we demonstrate that memory CD4 T cell-driven secondary responses to influenza challenge result in improved viral clearance yet do not prevent the morbidity associated with viral infection, and they exacerbate cellular recruitment into the lung, compared with primary responses.

CTLA4 expression is an indicator and regulator of steady-state CD4+ FoxP3+ T cell homeostasis.

The presence of FoxP3(+) regulatory T cells (Tregs) is necessary for control of deleterious immune responses in the steady state; however, mechanisms for maintaining the frequency and quality of endogenous Tregs are not well defined. In this study, we used in vivo modulators of the CD28 and CTLA4 pathways administered to intact mice to reveal mechanisms controlling the homeostasis and phenotype of endogenous Tregs. We demonstrate that expression of the negative costimulatory regulator CTLA4 on FoxP3(+) Tregs in vivo is a direct consequence of their rapid, perpetual homeostasis.