interleukin-12 through interactions with macrophages, dendritic cells, and neutrophils (Meier & McCalmont, 2014). This response primes T cell activation and keeps the process continually in motion (Meier & McCalmont, 2014). Maladaptive and Physiological Responses SLE undergoes a range of relapses and remissions and can be challenging to diagnose and treat because patients exhibit different combinations of clinical manifestations such as skin rashes, oral ulcers, arthritis, seizures, psychosis, hemolytic anemia, leukopenia, thrombocytopenia, and renal failure (Moulton et al., 2017). Individuals with SLE have deficiencies in innate immunity causing tissue damage through malfunctioning phenotypes and functions of neutrophils, monocytes, macrophages, and dendritic cells that keeps apoptotic debris from being cleared away, an increase in self-antigens, and inflammatory cytokine production (Moulton et al., 2017). Type II and type III hypersensitivity reactions are noted in SLE. Type II hypersensitivity reacts against a specific cell by binding antibodies to an antigen on the cell surface that prevents or destroys normal functioning through five different mechanisms (Rote, 2017). These five mechanisms are complement-mediated lysis, clearance of macrophages in the tissue, neutrophil-mediated immune destruction, the release of toxic substances through antibody-dependent cell-mediated cytotoxicity, and cellular malfunction (Rote, 2017). In type III hypersensitivity, antibodies attach to soluble antigens that are distributed into blood or body fluids, then placed into tissues causing damage (Rote, 2017).
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