**1. Introduction**

Fungal infections are a serious public health concerns, particularly with the growing number of immunocompromised individuals. *C. albicans* amongst other fungal species has been identified as one of the leading cause of infections in recent times [1]. Candidemia and Candidiasis account for 50% and 70% prevalence infections in human and has caused a great deal of morbidity and mortality largely because of the polymorphic nature of *C. albicans*. Also, factors such as toxicity of antifungal drugs, drug resistance, limited arsenal of antifungal drugs, slow mycological diagnosis, variable drug bioavailability in immune-compromised patients and drug interactions have truncated every efforts being made at mitigating the prevalence and its consequential effects. These challenges have led to the several attempts at developing a viable preventive option for candida infections. The cellular surface of *C. albicans* is a predominant source of immuno-stimulatory antigens [2] comprising of 90% carbohydrates and 10% proteins [3] and hence making carbohydrates dominate immune recognition while the proteins exhibit the key role of adhesive interactions with the host cellular surfaces. Therefore, complete inactivation of the pathogen amongst many strategies such as using the genetic material, a specific protein on the cell surface or attenuation to prevent candidiasis has been attempted. The killed *C. albicans* has lost its ability to infect their hosts but can stimulate enough immunological responses for the host protection. White blood cells response against *C. albicans* is initiated within the first few hours of inoculation or infection.

Therefore during host – killed *C. albicans* interaction, the cell surface molecules trigger and modulate cell mediated (T cells) and innate immune cells (macrophages, neutrophils and natural killer cells) to respond appropriately. These cells

are considered to be the first line and most important defense mechanism against Candidiasis [4] and consequently induced a strong response against the pathogen [5]. These responses function synergistically, co-operate and modulate each other with the final goal of fighting infection (4).
