Example sentences for: autoreactive

How can you use “autoreactive” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • These non-physiologic RSS are important because of their potential involvement in oncogenic chromosomal translocation and receptor editing, a process that alters the specificity of autoreactive receptors.

  • Although direct evidence that autoantigen cleavage fragments produced during cell death elicit autoantibody responses is still scarce, Pollard et al . reported that immunization of B10.S mice (H-2 s) with a 19 kDa proteolytic cleavage fragment of fibrillarin (derived from nonapoptotic cell death) elicited antibodies that are comparable with human anti-fibrillarin autoantibodies and those derived from mice exposed to mercury [ 40 ] . In a study using human sera, Greidinger et al . reported that the recognition of apoptosis-derived and oxidatively modified forms of the 70 kDa subunit of U1 small nuclear ribonucleoprotein autoantigen was associated with distinct disease manifestations [ 41 ] . Furthermore, Oriss et al . demonstrated that a combination of antigen-processing cells and a fragment of DNA topoisomerase I efficiently elicited autoreactive T-cell proliferation, whereas the full-length topoisomerase I required additional stimulus of exogenous interleukin-2 [ 42 ] .

  • First, CD4 +T cells selectively proliferate in response to proteoglycan antigens [ 14 ] . Second, prevention of arthritis can be achieved by in vivo treatment with anti-CD4 monoclonal antibodies [ 15 ] . Third, arthritis can be transferred to naïve BALB/c or severe combined immunodeficient (SCID) mice using T and B cells from arthritic animals [ 16 17 18 ] . Fourth, a proteoglycan-specific T-cell hybridoma (T-helper-1 type) can induce arthritis in BALB/c mice [ 19 ] . Finally, CD4 +T cells from arthritic animals are resistant to activation-induced cell death [ 20 ] . These data suggest a breakdown of peripheral tolerance and accumulation of autoreactive T cells in the periphery.

  • In induced models of autoimmunity, the CD28-B7 interaction has been shown to regulate disease susceptibility by rendering autoreactive T cells anergic, or alternatively by upregulating the threshold for autoreactive T-cell activation [ 30 ] . Furthermore, we previously showed that impaired Fas-mediated activation-induced cell death (AICD) of autoreactive T-helper-1 cells may be responsible for the development of PGIA [ 20 ] . Therefore, AICD and/or T-cell anergy, but not the CD4 +CD25 +regulatory T cells, may be responsible for deletion or inactivation of autoreactive T cells in autoimmune arthritis.

  • Some of the autoreactive T cells, however, may escape from negative selection and are released into the periphery.


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