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000142744 1001_ $$aRaposo, Bruno$$b0
000142744 245__ $$aT cells specific for post-translational modifications escape intrathymic tolerance induction.
000142744 260__ $$a[London]$$bNature Publishing Group UK$$c2018
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000142744 520__ $$aEstablishing effective central tolerance requires the promiscuous expression of tissue-restricted antigens by medullary thymic epithelial cells. However, whether central tolerance also extends to post-translationally modified proteins is not clear. Here we show a mouse model of autoimmunity in which disease development is dependent on post-translational modification (PTM) of the tissue-restricted self-antigen collagen type II. T cells specific for the non-modified antigen undergo efficient central tolerance. By contrast, PTM-reactive T cells escape thymic selection, though the PTM variant constitutes the dominant form in the periphery. This finding implies that the PTM protein is absent in the thymus, or present at concentrations insufficient to induce negative selection of developing thymocytes and explains the lower level of tolerance induction against the PTM antigen. As the majority of self-antigens are post-translationally modified, these data raise the possibility that T cells specific for other self-antigens naturally subjected to PTM may escape central tolerance induction by a similar mechanism.
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000142744 650_7 $$2NLM Chemicals$$aAutoantigens
000142744 650_7 $$2NLM Chemicals$$aCollagen Type II
000142744 7001_ $$aMerky, Patrick$$b1
000142744 7001_ $$aLundqvist, Christina$$b2
000142744 7001_ $$aYamada, Hisakata$$b3
000142744 7001_ $$aUrbonaviciute, Vilma$$b4
000142744 7001_ $$aNiaudet, Colin$$b5
000142744 7001_ $$aViljanen, Johan$$b6
000142744 7001_ $$aKihlberg, Jan$$b7
000142744 7001_ $$0P:(DE-He78)08a57258198dcedd8ff8ac7eef40341a$$aKyewski, Bruno$$b8$$udkfz
000142744 7001_ $$00000-0002-4506-9955$$aEkwall, Olov$$b9
000142744 7001_ $$00000-0002-4969-2576$$aHolmdahl, Rikard$$b10
000142744 7001_ $$aBäcklund, Johan$$b11
000142744 773__ $$0PERI:(DE-600)2553671-0$$a10.1038/s41467-017-02763-y$$gVol. 9, no. 1, p. 353$$n1$$p353$$tNature Communications$$v9$$x2041-1723$$y2018
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