Joshua D. Ooi, A. Richard Kitching Kidney International

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CD4+ Th1 cells are effectors in lupus nephritis—but what are their targets? Joshua D. Ooi, A. Richard Kitching Kidney International Volume 82, Issue 9, Pages 947-949 (November 2012) DOI: 10.1038/ki.2012.254 Copyright © 2012 International Society of Nephrology Terms and Conditions

Figure 1 How Th1 cells may induce injury in lupus nephritis. (a) In lupus nephritis, antigens can be present in glomeruli as endogenous antigens (pink) that can be part of the extracellular matrix or associated with endothelial cells, podocytes, or mesangial cells (not shown here, for clarity). Alternatively, blood-borne lupus-related antigens can lodge within glomeruli (blue), either as free antigens or deposited as part of circulating immune complexes. (b) Autoreactive effector CD4+ Th1 cells recognize their cognate autoantigen (not shown here; there are several potential mechanisms) and adhere in glomeruli. Production of interferon-γ induces proinflammatory mediators such as chemokines and activates macrophages. Cell–cell contact via CD154/CD40 is also important, promoting macrophage activation. This lesion has some of the features of a delayed-type hypersensitivity-like reaction, occurring in the kidney and resulting in diffuse proliferative lupus nephritis. CD40L, CD40 ligand; GBM, glomerular basement membrane; Mac, macrophage. Kidney International 2012 82, 947-949DOI: (10.1038/ki.2012.254) Copyright © 2012 International Society of Nephrology Terms and Conditions