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Negative selection in T cell development is often simply described as preventing effector T cells from recognizing self-antigens. This is complicated by regulatory T cells developing from T cells with moderate affinity for self-antigens. If recognition of self is useful for immune tolerance, why don't T-cells with strong affinity for self-antigens also become regulatory T cells?

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The selection is based upon the strength of the binding. A strong bond causes a signal in the T-cell to self destruct (apoptosis).

Wikipedia has a post on T cells. Perhaps the moderate bonding become regulatory cells, because these cells have to recognize those T cells that survive negative selection, which are most likely to cause autoimmune responses over a long period of time.

Strong affinity to self means the immune response will become a danger to the host.

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  • $\begingroup$ I understand that effector cells should have a weak affinity for self so that they do not attack the host, but why shouldn't regulatory cells? If moderate affinity for self is used by regulatory cells for tolerance, why wouldn't strong affinity for self do the job better? $\endgroup$ – BatWannaBe Apr 11 '19 at 7:38
  • $\begingroup$ @BatWannaBe To my knowledge the strength of the self-reactivity of Tregs can differ by subset, and those cells have different roles. The problem, and some evidence here, is that high self-reactivity is associated with autoimmunity. $\endgroup$ – CKM Apr 11 '19 at 19:58
  • $\begingroup$ @CKM The article you linked seems to claim that higher self-reactivity makes Tregs better at SUPPRESSING autoimmunity. See the discussion paragraph starting with "Our study showed that the level of TCR self-reactivity alone can be used to identify superiorly functional Tregs in preventing tissue-specific autoimmunity." $\endgroup$ – BatWannaBe Apr 11 '19 at 20:32
  • $\begingroup$ @BatWannaBe Sorry, I was unclear and that comment was less helpful than when I was typing it up. They do state that clearly in the discussion. There are also some tidbits that continuous TCR signaling can potentially make the Tregs dysfunctional and ablate their ability to control the autoimmunity. $\endgroup$ – CKM Apr 11 '19 at 22:12

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