Abstract

A cross-sectional, correlational pilot study evaluating macrophage migration inhibitory factor (MIF) in plasma samples collected at early second trimester from 40 healthy pregnant women found a positive correlation between plasma MIF (ELISA) and plasma tyrosine (HPLC) ( r = 0.43, p < 0.008) levels. MIF functions as a proinflammatory cytokine, participates in glucocorticoid (e.g. cortisol) regulation via the MIF/glucocorticoid dyad, and is an increasingly important small molecule involved in modulation of neuroendocrine-immune crosstalk. Tyrosine motifs participate extensively in scaffolding phosphorylation and receptor/nonreceptor signaling; furthermore, nonreceptor tyrosine kinases have been shown to be activated by CD44, the signaling component of the MIF-CD74 complex. Potential key aspects of a correlation between MIF and tyrosine may be their mutual involvement in the persistence of B cells (a Th2 immune hallmark) with related survival signaling (e.g. MIF-CD74 induction), equilibrium in MIF glucocorticoid regulation, and a possible role in the Type 1 to Type 2 immune shift during pregnancy with resulting altered homeostasis and inflammation. Research suggests MIF and tyrosine levels may have a role in TLR-induced signaling directly bridging the innate to adaptive immune response (e.g. DAMP). Seemingly these factors also could demonstrate further significance when assessing pregnancy outcomes. In addition, expanded assessment of this correlation may illuminate specific mechanisms by which MIF and tyrosine in the periphery may cross the BBB and/or have a role in modulating neuroendocrine-immune interactions in the CNS.

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