Post by Max on Jul 13, 2005 5:54:34 GMT -5
Hypoimmunoglobulinemia - Lack of IgE response
Repeated studies, in both mice and human subjects show the lack of a primary IgE response with elevated and sustained secondary IgE responses during and after 13-cRA exposure [1 and more]. The recognition of allergy in subjects with hypoimmunoglobulinemia is very difficult because they have very low level or even lack of specific IgE antibodies. Sensitivity to cow's milk in 24 children and additionally in 4 of them sensitivity to gluten [2].
IgE binds to human insulin [3 and more], whereas it could be suspected that the natural anti-insulin responses are disrupted in subjects displaying partial or severe hypoimmunoglobulinemia. The SH2 domain proteins transmit intracellular signals initiated by activated tyrosine kinase-linked receptors, and are sensitive to IgE [4]. It is therefore a possibility that lack of IgE responses causes a disruption in Trk signaling.
Discussion
Significant research is done on the opposite condition, hyperimmunoglobulinemia, but little is known about long term effects in subjects with partial or severe deficits in IgE responses. It remains clear that the functions of IgE are wide and not fully discovered.
It is here suggested that lack of IgE response can alter insulin sensitivity by altering IgE mediated phosphorylation processes, and contibute to altering (decreasing) steroidal receptor binding affinity and lipid composition in cellular membranes.
Repeated studies, in both mice and human subjects show the lack of a primary IgE response with elevated and sustained secondary IgE responses during and after 13-cRA exposure [1 and more]. The recognition of allergy in subjects with hypoimmunoglobulinemia is very difficult because they have very low level or even lack of specific IgE antibodies. Sensitivity to cow's milk in 24 children and additionally in 4 of them sensitivity to gluten [2].
IgE binds to human insulin [3 and more], whereas it could be suspected that the natural anti-insulin responses are disrupted in subjects displaying partial or severe hypoimmunoglobulinemia. The SH2 domain proteins transmit intracellular signals initiated by activated tyrosine kinase-linked receptors, and are sensitive to IgE [4]. It is therefore a possibility that lack of IgE responses causes a disruption in Trk signaling.
Discussion
Significant research is done on the opposite condition, hyperimmunoglobulinemia, but little is known about long term effects in subjects with partial or severe deficits in IgE responses. It remains clear that the functions of IgE are wide and not fully discovered.
It is here suggested that lack of IgE response can alter insulin sensitivity by altering IgE mediated phosphorylation processes, and contibute to altering (decreasing) steroidal receptor binding affinity and lipid composition in cellular membranes.