Why Is the Patient Out of Breath? Collagen V(α1) and K-α1-Tubulin Take Center Stage in Lung Transplantation

Abstract

Largely driven by the problem of obliterative bronchiolitis, a major form of chronic allograft dysfunction, in the lung transplant patient, the twin topics of T helper 17 (Th17) cells and autoimmunity have finally entered into the mainstream of transplantation immunobiology research (1). In doing so, lung transplantation has raised fundamental new questions about self-tolerance and its stability, such as: (i) How is selftolerance disrupted so easily in the setting of lung transplantation?, (ii) What do the major self-antigens that are recognized by lung transplant patients during chronic rejection, Collagen type V (Col-V) (2) and K-alpha-1-tubulin (Ka1T) (3), have in common? (iii) Is this response an example of classical epitope spreading typical of a de novo autoimmune disease, or is it the result of a tissue homeostatic mechanism gone awry? and finally, (iv) Why the bias toward Th17?