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How this family of coiled-coil proteins becomes autoimmune targets remains to be determined.
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In several spontaneous models, the genetic abnormalities that cause the loss of tolerance must be expressed in those B cells that become autoimmune [ 3].
In addition, recent works suggest that the paranodal and juxtaparanodal axo-glial components could become autoimmune targets (see above) (Mathey et al., 2007; Derfuss et al., 2009).
Coiled-coil proteins may be exposed to the immune system as surface structures in aberrant disease states associated with unregulated cell death and could become autoimmune targets [ 30].
From the findings discussed above, it becomes clear that autoimmune tissue injury also relates to tissue specific responses during exposure to microbial molecules.
Taken together these data suggest that elevated BG levels, occurring when autoimmune diabetes becomes clinically manifest, specifically and selectively stimulate β-cell multiplication.
Autoantibodies may be found years before an autoimmune disease becomes clinically apparent.
With increasing age of patients, the female-to-male ratio for autoimmune diseases becomes more prominent.
One tantalizing hypothesis, which arises from elegant mouse work, is that changes in local vascular permeability might provide a route via which a systemic autoimmune propensity becomes focused on the synovium [72].
Our model shows that the pathologic dynamic regime in autoimmune conditions become stationary and makes the autoimmune process chronic but relapsing instead of progressive.
See related editorial by Lundberg and Venables, Post-translational modifications can create neo-antigens that become targets of autoimmune responses [ 1, 2].
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CEO of Professional Science Editing for Scientists @ prosciediting.com