The host’s natural immune response was the first line of protection against potentially harmful infections. Toll-like receptors (TLRs) were responsible for activating signals transduction pathways involved in host defense, inflammation, development, and the generation of inflammatory cytokines. Mutations in NEMO, IKBA, MyD88, and IRAK4 were examples of innate immunodeficiencies connected with dysfunctional TLR signaling. Other deficiencies in the innate immune system were linked to an increased risk of developing herpes simplex encephalitis, viral infections, mycobacterial illness, chronic mucocutaneous candidiasis, and epidermodysplasia verruciformis. Phagocytes and natural killer cells were both necessary components of the innate immune system; however, if there was a deficiency in either the quantity of these cells or their activity, it could lead to a cycle of persistent infections. Another essential component of the innate immune system is called the complement system. A complement deficiency could increase the risk of infection, autoimmune disease, or defective immune complex clearance. The innate immune system’s primary responsibilities include the rapid identification and destruction of infections, coordinating immune responses, and activating the adaptive immune system. Defects in the innate immune system could lead to an inability to recognize pathogens promptly and activate the immune response. This could result in a heightened risk of developing severe infections or illnesses that keep coming back.
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