Abstract
KIM-1/TIM-1 in proximal tubular cell immune response.
Highlights
Kidney injury molecule-1/T cell IgG and mucin containing 1 (KIM-1/TIM-1 formed a new class of proteins (TIMs)-1) is a type 1 membrane receptor [1] which we identified as the most upregulated proximal tubular cell (PTC) protein following a variety of kidney injuries in animal models and human diseases [1] (Figure 1A)
While KIM-1 ( known as hepatitis A virus cellular receptor-1 (HAVCR-1)) quickly was recognized as a promising biomarker, other proteins were subsequently discovered which, together with KIM-1/ TIM-1 formed a new class of proteins (TIMs) whose function was unknown at the time of discovery
As is often the case, identifying the function of KIM-1 only led to more questions: Why do non-myeloid cells express a scavenger receptor? Can PTCs efficiently phagocytose in vivo? What are the functional consequences of PTC phagocytosis? In other words, what is the role of KIM-1 in kidney injury?
Summary
Work from our lab identified KIM-1’s function as an apoptotic cell phosphatidylserine phagocytosis and scavenger receptor [2], whereby it induces the binding and uptake of dead cells from the kidney tubule lumen in acute kidney injury (AKI) (Figure 1B). Utilizing this novel animal model, we found that KIM-1 mediated phagocytosis is responsible for the clearance of much of the luminal apoptotic cells resulting from ischemic or nephrotoxic acute tubular injury [4].
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