Abstract
Major histocompatibility complex class one (MHC-I) antigen-presenting molecules participate in central nervous system (CNS) synaptic plasticity, as does the paired immunoglobulin-like receptor B (PirB), an MHC-I ligand that can inhibit immune-cells and bind to myelin axon growth inhibitors. Based on the dual roles of both molecules in the immune and nervous systems, we evaluated their expression in the central and peripheral nervous system (PNS) following sciatic nerve injury in mice. Increased PirB and MHC-I protein and gene expression is present in the spinal cord one week after nerve transection, PirB being mostly expressed in the neuropile region. In the crushed nerve, MHC-I protein levels increased 2 weeks after lesion (wal) and progressively decreased over the next eight weeks. The same kinetics were observed for infiltrating cytotoxic T lymphocytes (CTLs) but not for PirB expression, which continuously increased. Both MHC-I and PirB were found in macrophages and Schwann cells but rarely in axons. Interestingly, at 8 wal, PirB was mainly restricted to the myelin sheath. Our findings reinforce the participation of MHC-I and PirB in CNS plasticity events. In contrast, opposing expression levels of these molecules were found in the PNS, so that MHC-I and PirB seem to be mostly implicated in antigen presentation to CTLs and axon myelination, respectively.
Highlights
The major histocompatibility complex (MHC) is encoded by a polymorphic gene locus responsible for the transduction of antigen-presenting molecules, such as the human leucocyte antigen (HLA) and the histocompatibility molecules in mice (H)
One example is the Major histocompatibility complex class one (MHC-I) molecule, widely known to present antigens to cytotoxic T lymphocytes (CTLs), which has been shown to be involved in central nervous system (CNS) plasticity events [26, 27]
The importance of MHC-I for synapse refinement was first suggested by Huh and co-workers [4], who reported a surplus of retinogeniculate projections in mice lacking functional MHC-I molecules during development
Summary
The major histocompatibility complex (MHC) is encoded by a polymorphic gene locus responsible for the transduction of antigen-presenting molecules, such as the human leucocyte antigen (HLA) and the histocompatibility molecules in mice (H). Previous studies have shown that MHC-I molecules are expressed in the CNS during different phases of development [4] and aging [5] as well as after injuries [6, 7] In this sense, Oliveira and colleagues [8] reported the importance of MHC-I expression for the maintenance of inhibitory synapses opposed to axotomized alpha-motorneurons. Subsequent studies corroborated the involvement of MHC-I molecules in synaptic plasticity In this sense, the upregulation of MHC-I induced by IFN-β interfered with the synaptic reactivity and increased astroglial response in the spinal cord [7], as well as improved axonal growth and motor function recovery [6], following peripheral nervous system (PNS) damage. To date, the precise role of MHC-I in CNS/PNS plasticity is not fully understood
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