Words similar to autoimmunity
Example sentences for: autoimmunity
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Simple and accurate methods exist to determine for a single pair of alleles how the three possible genotypes (2 homozygotes and one heterozygote) affect disease outcome, and these methods have been used frequently in the literature on autoimmunity and HLA [ 28 29 30 ] and once (to our knowledge) in the HLA-infectious disease literature [ 33 ] . It is of additional interest for epidemiologists, immunologists, vaccine designers and evaluators, and population geneticists to know whether HLA heterozygosity in general improves the immune response to and outcome of infectious diseases.
Second, if this actually leads to autoimmunity, it also predicts that the initial break in tolerance that leads to disease should involve an X-linked autoantigen that is expressed in a peripheral nontolerizing site or circumstance.
Although it has been shown that the CD4 +CD25 +regulatory T cells can suppress the development of autoimmunity, a recent report [ 27 ] demonstrated that depletion of the CD4 +CD25 +T cells is necessary but not sufficient for induction of autoimmune gastritis.
Recently, a subset of CD4 +T cells was identified that is present on 5-10% of CD4 +T cells in normal naïve mice and expresses CD25 (the α-chain of IL-2 receptor) [ 4 5 ] . Functional analysis of murine CD4 +CD25 +T cells showed that those cells, which constitutively express cytotoxic T-lymphocyte antigen (CTLA)-4 [ 6 7 8 ] , fail to proliferate or secret cytokines in response to polyclonal or antigen-specific stimulation, but inhibit the activation of conventional responsive T cells [ 1 2 3 8 9 ] . The suppressive activity of the CD4 +CD25 +T cells depends on signaling via the negative regulator of T-cell activation CTLA-4 [ 7 ] and requires a cell-cell interaction that possibly involves cell surface bound transforming growth factor (TGF)-β 1 [ 1 10 ] . It has been shown that B7/CD28 costimulation is essential for the development and homeostasis of the CD4 +CD25 +regulatory T cells [ 6 ] , which play critical roles not only in preventing autoimmunity but also in controlling tumor immunity and transplantation tolerance [ 2 11 ] .
The results do not provide support for a major role for skewed X-chromosome inactivation in female predisposition to autoimmunity; however, neither is the underlying hypothesis disproved by our data.