Abstract
Systemic lupus erythematosus (SLE) is a multisystem inflammatory and autoimmune disorder that usually affects various self-tissues of the body, whose sera is predominantly reported to have autoantibodies against Ro60 or TROVE-2 protein. Ro60 is a ring-shaped RNA-binding protein, that usually binds misfolded non-coding RNAs, pre-5S rRNA, and several small cytoplasmic RNA molecules known as Y RNAs (hY-RNAs). Y RNAs are known to be involved in regulating cellular stress responses and also in initiation of chromosomal replication. Ro60 is known to have 6 isoforms along with the short isoform. Recent studies of Ro60 protein in mammalian cells suggests that Ro60 is vital for the cell survival after the UV irradiation. It is evident that Ro60 is essential for degrading the damaged RNA due to the UV irradiation, because exposure to the UV irradiation might result in RNA: RNA and RNA: Protein crosslinks. Also, role of Ro60 in maintaining the tolerance is supported by the experiment which resulted in development of lupus like syndrome in the Ro60 knock-down mice by producing antibodies against chromatin and ribosomes. Thus, it is evident from the various studies that Ro60 is inevitably important for the cells and tissues for preventing the autoimmunity. This review focusses on the pathology and autoantibody system in SLE, structure and functions of the Ro60 in association with Y RNAs, and epitope bindings of Ro60 to the anti-Ro positive sera from SLE patients.
Highlights
Systemic lupus erythematosus (SLE) is a multisystem inflammatory and autoimmune disorder that usually affects various self-tissues of the body, whose sera is predominantly reported to have autoantibodies against Ro60 or TROVE-2 protein
Smith and Germolec [2] stated that immunocompetent T-lymphocytes usually develop and mature in the thymus and can recognise the antigens only when processed into peptide fragments and are presented as bound to specialised surface molecules called as Major histocompatibility complex (MHC) proteins
As all the antigens that lymphocytes need to be tolerant of are not expressed in the central lymphoid organs, there are additional tolerance mechanisms that restrains the lymphocytes that are reactive to the self-antigens that are not expressed in the central lymphoid organs, such tolerance mechanisms that act on the mature circulating lymphocytes in the peripheral lymphoid organs is referred to as “peripheral tolerance [8].”
Summary
The concept of immunity came into existence with the scenario of plague infection in Athens in 430 BC, where the writings of a great historian stating “only those who had recovered from the plague could nurse the sick” gave an initial insight into the topic of immunity, by following a notion that the recovered ones does not develop the disease a second time [1]. T-lymphocytes and B-lymphocytes are further divided into sub populations based on the different functional properties, maturation, and activation [2] These sub populations of T-lymphocytes and B-lymphocytes are the crucial immune components to evoke an adaptive immune response. Smith and Germolec [2] stated that immunocompetent T-lymphocytes usually develop and mature in the thymus and can recognise the antigens only when processed into peptide fragments and are presented as bound to specialised surface molecules called as Major histocompatibility complex (MHC) proteins. B-lymphocytes can recognise the antigens via membrane bound antibody termed as immunoglobulin (Ig) which acts as antigen receptors [2] The regulation of these interactions between the immune cells and cell products during both the types of immune responses is necessary for the optimal functioning of the immune system [6]
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