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During pregnancy some cells traffic between the fetus and mother and recent studies indicate low levels persist in the respective hosts decades later. Microchimerism (Me) refers to a small population of cells or DNA harbored by one individual that derive from a genetically distinct individual. Persistent Me can also arise from cell transfer between twins in utero or after a blood transfusion. Because women are preferentially affected by autoimmune disease, often with an increased incidence in post-reproductive years, fetal Me has been investigated in diseases such as systemic sclerosis (SSc), autoimmune thyroiditis, primary biliary cirrhosis, Sjögren's syndrome and systemic lupus erythematosus. Maternal Me has been investigated in SSc, myositis and neonatal lupus. Evidence implicating fetal Me is strongest in SSc where quantitatively higher levels of fetal Me have been found and particular human leukocyte antigen (HLA) relationships of mother and child are associated with increased risk of subsequent SSc in the mother. Maternal Me is implicated in myositis and neonatal lupus. It is unknown how Me might be involved in autoimmune disease. Me could play a role in the effector arm of immune responses either directly or indirectly. Microchimeric cells could be targets of an immune response, an intriguing possibility suggested by a recent study in which maternal cells identified in hearts of infants with neonatal lupus congenital heart block were predominantly cardiac myocytes. Alternatively microchimeric cells could be recruited secondarily to diseased tissues and function in tissue repair. The long-term consequences of naturally acquired Me deriving from pregnancy are not yet known. Because persistent fetal and maternal Me are not uncommon in healthy individuals it seems likely that beneficial effects may also accrue to the host. Recent advances in this active frontier of scientific research are discussed. [ABSTRACT FROM AUTHOR]

The autoimmune rheumatologic diseases discussed in this chapter include rheumatoid arthritis (RA), systemic sclerosis (SSc), also called scleroderma, and systemic lupus erythematosus (SLE). Historically the terms connective-tissue diseases or collagen-vascular diseases have sometimes been used in considering diseases such as RA, SSc and SLE, because fibrinoid degeneration especially in collagen and vascular tissues is often found and was thought to contribute to clinical manifestations of these disorders. The predominant current view is that autoimmunity underlies the pathogenesis of these disorders, with normal tissues, cells and proteins the target of self-directed immune reactivity. Genetic susceptibility to autoimmune rheumatologic diseases is clearly multifactorial involving combinations of many different genes. More than three decades of research, however, indicates HLA genes most often make the strongest genetic contribution. Although the mechanism(s) by which particular HLA genes increase or decrease risk of a disease are not known it is not difficult to appreciate a central role since the products of HLA genes, HLA molecules, are intimately involved in the process of presenting both foreign and self antigens to T cells. For some diseases very specific HLA sequences have been identified and for others extended stretches of genes within the greater major histocompatibility complex (MHC) are implicated. More recently candidate genes other than those in the MHC have been identified for RA, SSc and SLE. Some implicated genes are known to be involved in other aspects of immune regulation while for other candidate genes the functions are as yet unknown. [ABSTRACT FROM AUTHOR]