The major histocompatibility complex (MHC) is responsible for binding peptide fragments arising from pathogens in order to display them on the cell surface for recognition from immune cells. Once recognized, the foreign pathogen is typically evaded. The MHC complex is broken into two categories, MHC Class I proteins and MHC Class II proteins. MHC complex I and II proteins are all very different and contain specific molecules to bind different peptides – in fact, they have been described as the most polymorphic genes there are. The MHC Class II RT1B antibody can be used to bind the monomorphic determinant of the rat I-A antigen, which is found on B-lymphocytes, dendritic cells and some macrophages. Often times, a neuroinflammatory response develops after brain injury and remains for weeks post injury. Using a MHC Class II RT1B antibody is a useful way to understand our immune response post brain injury.
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MHC Class II RT1B Antibody (OX-6) [NB100-65541] - IHC analysis of a formalin fixed and paraffin embedded tissue section of mouse spleen using MHC Class II RT1B antibody (clone OX-6) at 1:100 dilution. The signal was developed using HRP-labelled secondary antibody and DAB reagent, and the nuclei were counterstained with hematoxylin. The antibody generated very specific signal in a subset of spleenocytes.
Kuric et al used a MHC Class II RT1B antibody to study the dynamics of MHC Class II positive cells in the post-ischemic brain and how a levodopa treatment influenced this activity. Male Sprague Dawley rats were subjected to brain injury in the form of transient occlusion of the middle cerebral artery (tMCAO) followed by a levodopa treatment. From here, the MHC II+ cells were analyzed in flow cytometry, western blot and immunocytochemistry using primary antibodies. The MHC Class II RT1B antibody was used in immunocytochemistry of paraformaldehyde fixed-brain sections and showed a reduction in protein expression 14 days after tMCAO. Likewise, using the MHC Class II RT1B antibody in western blot on levodopa treated vs control brain tissue samples also showed reduced expression of the MHC Class II protein. Ultimately this research does suggest that the levodopa treatment reduces MHC II+ cells post brain injury.
Next, Barreto et al used a MHC Class II RT1B antibody to elucidate the role of estrogen receptor modulators in regulating reactive microglia after brain injury. One method of neuroinflammation post brain injury can arise in the form of reactive microglia that can become dangerous. Once again, the MHC Class II RT1B antibody was used in this research to label MHC II+ microglial cells post injury in order to better understand their dynamics. Specifically, this type of antibody was used in immunohistochemistry of brain injury tissue samples. This group found that sections surrounding the brain injury wound were lined with MHC II+ microglia, and that animals treated with estradiol had a reduction in this cellular density.
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