A growing number of studies has demonstrated the involvement of the major histocompatibility complex class I (MHC-I) molecules in distinct processes of antigen presentation to the cytotoxic T cells (T CD8) of the immune system. Although the expression of MHC-I molecules by neurons is low in basal conditions, it has been demonstrated that these cells are able to significantly enhance the expression of MHC-I under injury as well as during certain stages of the embryonic development. Besides the classic receptor of MHC-I is present on T cells (TCR), there are also other molecules that bind to MHC-I, among them the Paired immunoglobulin-like receptor B (PIR-B), with inhibitory activity, which is present in different immune cells as well as in the projections of neurons under injury or during the embryonic development. Some peripheral nerve injuries can trigger retrograde cellular responses in the spinal cord, such as chromatolysis of axotomized neurons accompanied by an increased astrocytic reactivity, and in these cases, astrocytes may act in the synapse striping of those damaged neurons, which can also overexpress MHC-I. It is worth to mention that peripheral lesions do not evoke inflammation in the spinal cord, as so the MHC-I molecules expressed in sites that are distant from the lesion do not act in the process of immune surveillance. In view of the above, this project proposes to assess the involvement of MHC-I molecules and their ligand PIR-B in the process of astrocytic reactivity in the spinal cord of mice that were submitted to the sciatic nerve transection.
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