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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.
The question of how we acquire immunity has been investigated for a century or more. What have we learned from all of this endeavor? We asked Rolf Zinkernagel to provide, for the young investigator, food for thought about that which we still don't know—even if we think we do.
