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It is becoming more apparent that some B cells do not carry the same antigen receptors throughout their life. B cells that have edited their receptors have now been found in humans as rare cells that accumulate in arthritic joints.
The complement inflammatory cascade is crucial to our innate ability to ward off infection. Two papers now provide evidence linking C5 and C3a to murine airway hyperresponsiveness, a partial model of human asthma. Surprisingly, these complement proteins appear to have opposite effects.
T cell activation usually requires TCR engagement by antigen and another, costimulatory, signal. Modeling studies now indicate that this second signal may only slightly enhance TCR signaling, but nevertheless results in an exponential increase in cell numbers.
The proto-oncogene BCL6 participates in the regulation of immune responses; a lack of it leads to generalized type 2 inflammation. Macrophage chemokine genes have now been identified as targets for BCL-6 repression and perhaps induce this inflammation.
How do T cells that are specific for pancreatic islet cell antigens cause diabetes? A recent paper in Nature provides evidence from NOD mice that the killer T cells responsible increase their avidity as the disease progresses—removing the high avidity clones prevents disease.
Perturbation of T cell differentiation by overexpression of SCL and LMO can lead to leukemia. This dysregulation may be initiated by inactivation of E2A.
Much vaccine research is directed toward the generation of more effective vaccines. By combining DNA vaccines with the innate immune system, a flu vaccine was designed that required only a single immunization.
Tumor vaccines comprised of the chaperone gp96 can instigate specific immunity to tumor peptides. A receptor on macrophages for the uptake of peptide-loaded gp96 has been identified as CD91, the α2-macroglobulin receptor.
NK cells become cytotoxic upon receiving a signal through their activation receptors. The orphan proteins H-60 and Rae1 have now been identified as ligands for the mouse NKG2D activation receptor. Remarkably they are inducible and may be blocked by a viral protein.
Protection of the small intestine from harmful bacteria is a never-ending job. Paneth cells of the intestinal crypts function as prime producers of defensins in response to the microbial onslaught of the gut.
Memory is generated with most T cell responses. The effectiveness and power of CD8+ memory T cells may be due to their quicker responses and broader capabilities.
Without Brca1, T cells are lacking in numbers and maturity, but surprisingly not because of a lack of repair of rearranged TCR genes. The defects involve more than one p53-dependent mechanism.
STATs are critical in immune responses to type 1 IFNs. The human and mouse pathways differ, partly due to differences in STAT2, but unpredicted responses after viral infections raise new questions.
Marginal zone B cells may steal the limelight as the roles of Pyk-2 and BLyS begin to be elucidated. Pyk-2 deficiency leads to their loss whereas signaling via the BLyS receptor may augment their function.
The enzyme cPLA2 plays a pivotal role in adult respiratory distress syndrome (ARDS). Specific blocking of cPLA2 may present a useful therapeutic target for treating ARDS.
