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Expression and in vitro upregulation of MHCII in koala lymphocytes

Lau, Q, Canfield, PJ & Higgins, DP 2012, Veterinary Immunology and Immunopathology, vol. 147, pp. 35-43.

The purpose of this study was to characterise class II major histocompatibility complex (MHCII) in koalas in terms of abundance and distribution between sexes and seasons, and further to evaluate MHCII as a marker of lymphocyte activation during in vitro studies. Flow cytometry found that the expression of MHCII was upregulated within activated B lymphocytes in cell culture, but not koalas with active inflammation. Furthermore, MHCII was found to be expressed predominantly on circulating B lymphocytes rather than on T lymphocytes.

  Dual-labelled flow cytometry was carried out on whole blood samples from koalas, as well as isolated samples of peripheral blood mononuclear cells (PBMCs) with mitogen stimulation, using antibodies targeting intracellular epitopes of T and B lymphocytes and MHCII epitopes. Absolute B lymphocyte numbers were observed to be higher compared to T lymphocytes, with the majority of MHCII-labelling occurring on the B lymphocytes. The expression of MHCII was found to be not affected by sex or season; however, circulating T and B lymphocyte concentrations were seen to increase for females but decrease for males in summer, and the reverse in autumn. Mitogens stimulated the expression of MHCII on B lymphocytes, but not on T cell lymphocytes. Furthermore, the in vitro upregulation of MHCII was not mirrored in koalas undergoing natural inflammation. Comparison of healthy and diseased koalas found no difference between the number of MHCII+ B lymphocytes within the two groups.

  While in vitro mitogen stimulation resulted in the higher expression of MHCII on B lymphocytes, this was not mirrored in koalas with active inflammation. It is not entirely clear why this is so and limits the potential of MHCII expression as an in vitro marker for in vivo immunity studies. The reason for the low MHCII expression levels on T cell lymphocytes in both in vitro and in vivo analyses is unclear in this study. It does suggest, however, that an alternative immune mechanism or the higher abundance of circulating MHCII-expressing B lymphocytes may compensate for this. It should be noted that in this study, other than an observation of clinical signs, no molecular analysis was conducted to confirm if the inflammatory response was due to an infectious agent.

  The findings of this study conclude that the stimulation of MHCII expression are of unequal magnitude between in vitro and in vivo studies. This warrants further investigation to find a suitable indicator with a marked change in both laboratory and natural settings. Furthermore, understanding why activated T lymphocytes have a low expression of MHCII may be important in relation to the other unusual aspects of the koala adaptive immune response.

 

Summarised by Daniel Chew

 

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