The phrase "autoimmune pathology" is correct and usable in written English.
It can be used in medical or scientific contexts to refer to diseases or conditions that arise from an abnormal immune response against the body's own tissues.
Example: "Research into autoimmune pathology has revealed new insights into the mechanisms behind diseases like lupus and rheumatoid arthritis."
Alternatives: "autoimmune disease" or "autoimmune disorder".
The notion that mimicry between a self and a microbial peptide antigen can trigger or aggravate autoimmune pathology remains a popular hypothesis in autoimmunity research.
Taken together, we show that engineered clonal MBP-specific Tregs are able to suppress autoimmune pathology in EAE.
These regulatory cell populations can prevent harmful inflammation following completion of protective responses and thwart the development of autoimmune pathology.
Autoimmune pathology develops upon activation of autospecific conventional T cells (Tconv) and suppression of these immune-responses involves autospecific Treg (Kieback et al., 2016; Yang et al., 2015).
Treg therefore prevent the development of autoimmune pathology and chronic inflammation in interfaces with the environment such as the intestines, lungs, and skin.
The latter data indicated that a lack of Treg or Treg-functional capacity was responsible for the lymphoproliferation and lethal autoimmune pathology in mutant mice.
In the presence of anti-DFS70 antibodies (possibly confirmed with specific tests), it should be indicated that said marker "does not generally correlate with ANA-associated autoimmune pathology".
We will discuss how and where these distinct signals intersect to drive development of a Treg repertoire which efficiently protects the organism from autoimmune pathology.
However, it should be kept in mind that B cell responses and antibodies also have important regulatory roles in limiting autoimmune pathology.
It therefore appears appealing to postulate that Treg preventing autoimmune pathology develop mostly in the thymus where autospecific T cell precursors can recognize self-antigens presented by thymic stromal cells (Klein and Jovanovic, 2011).
Though intriguing, these results will need to be reconciled with the observation that transgenic expression of Foxp3 restored Treg development and prevented autoimmune pathology in IL-2Rβ deficient mice (Soper et al., 2007).
