Volume 12 Issue 6, June 2011

Naive lymphocytes have a finite lifespan and are continually replaced by input from generative organs. In contrast, memory cells or their progeny can last a lifetime. The expanded populations of memory cells and their more widespread distribution provide protection against recurrent infection.

The transcription factor BATF directly regulates key components of the formation and function of follicular helper T cells and antibody class switching in B cells.

Identification of the pathogenic cytokines that underlie the IL-23-dependent disease progression of experimental autoimmune encephalomyelitis has proven elusive. Evidence now points to GM-CSF.

The transcription factor Foxp1 helps maintain the quiescence of naive T cells by inhibiting IL-7Rα expression and diminishing signaling by the kinase Erk.

The contribution of basophils to allergic and helminth immunity remains unclear. Locksley and colleagues use reporter strains and two-photon microscopy to demonstrate that basophils do not mediate T helper type 2 priming in vivo.

The transcription factor BATF is known to control switched antibody responses. Murphy and colleagues show that BATF functions at multiple hierarchical levels in follicular helper T cells and B cells to regulate these responses.

The molecular mechanisms that underlie T cell quiescence are poorly understood. Hu and co-workers show that the transcription factor Foxp1 has an essential cell-intrinsic role in regulating the quiescence of naive T cells.

IL-2 is well known for its effects on the proliferation of T cells. Leonard and colleagues demonstrate a mechanism in which IL-2 is critical for supporting T_H1 differentiation but blocks T_H17 differentiation.

The development of experimental autoimmune encephalomyelitis has been attributed to cells of the T_H1 or T_H17 subset of helper T cells. Becher and Rostami and their colleagues show that IL-23-induced production of the cytokine GM-CSF underlies disease development and severity.

The development of experimental autoimmune encephalomyelitis has been attributed to cells of the T_H1 or T_H17 subset of helper T cells. Becher and Rostami and their colleagues show that IL-23-induced production of the cytokine GM-CSF underlies disease development and severity.

Seven specially commissioned articles and an overview survey the topic of immunological memory.