This review attempts to cover the implication of the toll-like receptors (TLRs) in controlling immune functions with emphasis on their significance, function, regulation and expression patterns. The tripartite TLRs are type I integral transmembrane receptors that are involved in recognition and conveying of pathogens to the immune system. These paralogs are located on cell surfaces or within endosomes. The TLRs are found to be functionally involved in the recognition of self and non-self-antigens, maturation of DCs and initiation of antigen-specific adaptive immune responses as they bridge the innate and adaptive immunity. Interestingly, they also have a significant role in immunotherapy and vaccination. Signals generated by TLRs are transduced through NFκB signaling and MAP kinases pathway to recruit pro-inflammatory cytokines and co-stimulatory molecules, which promote inflammatory responses. The excess production of these cytokines leads to grave systemic disorders like tumor growth and autoimmune disorders. Hence, regulation of the TLR signaling pathway is necessary to keep the host system safe. Many molecules like LPS, SOCS1, IRAK1, NFκB, and TRAF3 are involved in modulating the TLR pathways to induce appropriate response. Though quantification of these TLRs helps in correlating the magnitude of immune response exhibited by the animal, there are several internal, external, genetic and animal factors that affect their expression patterns. So it can be concluded that any identification based on those expression profiles may lead to improper diagnosis during certain conditions.

Heat stress affects the fertility and reproductive livestock performance by compromising the physiology reproductive tract, through hormonal imbalance, decreased oocyte quality and poor semen quality, and decreased embryo development and survival. Heat stress decreases the secretion of luteinizing hormone and estradiol resulting in reduced length and intensity of estrus expression, increased incidence of anoestrus and silent heat in farm animals. Oocytes exposed to thermal stress lose its competence for fertilization and development into the blastocyst stage, which results in decreased fertility because of the production of poor quality oocytes and embryos. Furthermore, low progesterone secretion limits the endometrial functions, and subsequently embryo development. In addition, the increased secretion of endometrial prostaglandin F2 alpha during heat stress threatens the maintenance of pregnancy. In general, the percentage of conception rate was found to be reduced by 4.6% for each unit increase in temperature humidity index (THI) above 70, and heat stress during pregnancy further slows down the growth of the foetus and results in lower birth weight. In tropical and subtropical regions, during hot days, the testicular temperature may increase and impair both the spermatogenic cycle and semen quality, which culminates in decreased bull fertility. The effects of heat stress on livestock can be minimized via adapting suitable scientific strategies comprising physical modifications of the environment, nutritional management and genetic development of breeds that are less sensitive to heat stress. In addition, the summer infertility may be countered through advanced reproductive technologies involving hormonal treatments, timed artificial insemination and embryo transfer, which may enhance the chances for establishing pregnancy in farm animals.

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