**4. Immunology at a glance**

There are two major groups of immunity in the human body—innate and adaptive immune responses. Innate immunity comprises immune responses which do not require the previous contact with immune triggers [6, 18]. The response is rapid but not specific and has no memory [18]. Innate immunity acts as the first line of defense against harmful substances. Activation of the innate immune system may eliminate the substance and trigger inflammation by releasing mediators such as cytokines, reactive oxygen species, and nitric oxide [6]. Elimination may also be carried on by cell-dependent mechanisms, such as phagocytosis and cytotoxicity [18]. In the gastrointestinal tract, mucosal defense is classified as an innate immune system that consists of mucosal epithelium, gastric acid, and immune cells (macrophage and dendritic cell) [1, 18]. The innate cellular immune may sense the presence of antigen via pattern recognition receptors (PRR), such as toll-like receptors (TLR) [18].

Adaptive immunity is an immune response toward previously contacted immune triggers. This immune system is specific and has immunologic memory. Activation of adaptive immunity is related to innate immunity. For example, antigen-presenting cells (macrophages and dendritic cells), as a part of the innate immune system, trigger activation and differentiation of T-helper (Th) cells, which marks the initiation of the adaptive immune response [6]. Th cells differentiate into Th1, Th2, Th17, and regulatory T (Treg) cells. Th1 plays role in cell-mediated immunity while Th2 in humoral immunity [4–7]. The balance between Th1 and Th2 is important in maintaining a normal host's immune response [6]. Th1 cells secrete tumor necrosis factor (TNF) and interferon (IFN)γ. Th2 cells secrete interleukin (IL)-4, IL-5, and IL-10 which act in suppressing the inflammatory effect of Th1 and in producing antibodies by lymphocyte B cells [3–5, 7]. Th17 plays role in the immune response toward extracellular bacterial infection by secreting IL-17A, IL-17F, IL21, and IL-22. Treg itself has activity in suppressing effector T cells proliferation and cytokine production, therefore moderating inflammation and preventing autoimmunity. Some cytokines secreted by Th17 are IL-10 and transforming growth factor (TGF)-β [3–5].
