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Effector CD4T cells recognize intravascular antigen presented by patrolling monocytes.

Effector CD4T cells recognize intravascular antigen presented by patrolling monocytes.
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Westhorpe CLV, Norman MU, Hall P, Snelgrove SL, Finsterbusch M, Li A, Lo C, Tan ZH, Li S, Nilsson SK, Kitching AR, Hickey MJ,


Westhorpe CLV, Norman MU, Hall P, Snelgrove SL, Finsterbusch M, Li A, Lo C, Tan ZH, Li S, Nilsson SK, Kitching AR, Hickey MJ, (click to view)

Westhorpe CLV, Norman MU, Hall P, Snelgrove SL, Finsterbusch M, Li A, Lo C, Tan ZH, Li S, Nilsson SK, Kitching AR, Hickey MJ,

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Nature communications 2018 02 219(1) 747 doi 10.1038/s41467-018-03181-4

Abstract

Although effector CD4T cells readily respond to antigen outside the vasculature, how they respond to intravascular antigens is unknown. Here we show the process of intravascular antigen recognition using intravital multiphoton microscopy of glomeruli. CD4T cells undergo intravascular migration within uninflamed glomeruli. Similarly, while MHCII is not expressed by intrinsic glomerular cells, intravascular MHCII-expressing immune cells patrol glomerular capillaries, interacting with CD4T cells. Following intravascular deposition of antigen in glomeruli, effector CD4T-cell responses, including NFAT1 nuclear translocation and decreased migration, are consistent with antigen recognition. Of the MHCIIimmune cells adherent in glomerular capillaries, only monocytes are retained for prolonged durations. These cells can also induce T-cell proliferation in vitro. Moreover, monocyte depletion reduces CD4T-cell-dependent glomerular inflammation. These findings indicate that MHCIImonocytes patrolling the glomerular microvasculature can present intravascular antigen to CD4T cells within glomerular capillaries, leading to antigen-dependent inflammation.

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