Candida species are a normal human flora in humans' digestive and reproductive systems, oral cavity, skin, and mucosal surfaces. Candida sp. is found in healthy people and can cause human infection during impaired immunity. Candida genus includes more than 100 different species. However, only a few can infect humans [26]. The community of healthy people has Candida sp. in the oral, gastrointestinal system,and vagina. Candida sp. is colonized and commensalism the mucosal and skin surfaces of humans and the urinary system [4], [3], [32].

Moreover, Candida albicans represent the prevalent opportunistic infection in the mucous membranes and skin. In addition, it is challenging to eliminate infection in immunocompromised people and those with diabetes [20]. One epidemiological study showed that 29 % (35 patients out of 120 samples) of Iraqi pregnant women were infected with Candida in the vagina. Those patients have a history of receiving antibiotics, and contraceptive medications, and also have diabetes, and other diseases [5]. In another Iraqi study, 62 patients out of 160 samples of pediatric patients 62 were positive infection of Candida spp.(38.8 %) ([7].

Moreover, the indiscriminate use of antimicrobial drugs in COVID-19 patients has led to the emergence of multidrug-resistant fungal pathogens [2]. Previous clinical studies suggest that individuals with prior antibiotic treatment (30–45 %) were more likely to develop Candida infections (Shastri et al., 2020). Antibiotic-induced intestinal dysbiosis and immune dysregulation of host defenses increase the susceptibility of Candida to colonization and invasion of the intestine [35].

Innate immunity cells play a role as mediators to offensive microorganisms via phagocytosis. Neutrophils and macrophages are essential cells that inhabit target tissue and organs to destroy fungi via phagocytosis. The antifungal cells liberate antimicrobial materials including ROS (Reactive Oxygen Species), releasing inflammation signals involving chemokines and cytokines, that are main to induct immunity cells into the infection site [19]. Immunoglobulin A is considered a viaduct between the natural and adaptive immune. IgA is stimulated chiefly in reaction to colonizing with commensal microorganisms consequently preserving homeostasis by immune exemption. The generation of antibodies in mucosa membranes, especially IgA, via B-cells that inhabitant in tissue is essential to control the microbiome composition. IgA represents the predominant isotype antibody in the mucosal immunity system, prevalent in the gastrointestinal system, respiratory system, vagina, saliva, colostrum, and tear [31].

Immunoglobulin G antibodies have broad specificity against bacteria in the intestine which are a significant element in protecting the host against systemic bacterial infections [6]. Furthermore, IgG responses to different enteric fungi and their cellular wall elements are renowned to happen through gastrointestinal diseases [28] and understood as markers of diseases more than protection responses [21]. In a previous study, Candida albicans IgG was detected by ELISA and the outcomes indicated the presence IgG antibodies in 62.8 % of the infected women with Vulvovaginal candidiasis [24].

IL‐17 stimulates the induction, chemotaxis, and development of neutrophils, further driving the creation of anti-microbial peptides, that have a significant role in the immunity response toward Candida [11]. The adaptive immunity cells including Th 17 and Th 1 cells found to assist in the removal of fungi via organizing the phagocytic cell functions([41].

Notwithstanding the significance of Candida albicans in the pathology of humans, little information is known about the mechanisms by which the fungus is distinguished by the immunity cells and induces the host defenses. Toll-like receptor 2 (TLR2) and TLR4 are the main receptors to recognize Candida [34].

TLRs (Toll-like receptors) contribute to the recognition of fungi like Candida albicans. The relation between TLRs and yeast in Candida infection induces immunity cells to produce inflammatory and immunomodulation mediators that cause the immunity response. TLR2 distinguishes blastoconidia, and the hyphal shape of C. albicans [33].

One study confirmed that TLR2 −deficiencies in mice enhance inflammation in the intestine, and increase growth for C. albicans in colitis, indicating the role of TLR2 in epithelium homeostasis [12]. So that this study aimed to detect the immunological role of Candida infection by using some immunological markers.