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1.1 T helper cell subset Helicobacter pylori (H. pylori) and smoking are well known risk factors for gastric ulcer, and both are classified as definite carcinogens. Interestingly, the two also reportedly share common immune response features. With recent advances in immunology, various functions of T lymphocytes (T cells) have been discovered. T cells are divided into suppressor and helper on the basis of immunological functionings, and T helper cells are now known to consist of two distinct groups, as demonstrated using mouse models in the 1980s [Reiner, 2008; Mosman & Coffman, 1989]. Both groups are derived from naive T cells: interleukin-12 (IL-12) causes naive T helper cells to differentiate into type 1 (Th1) cells, while augmentation of IL-4 around naive T cells leads to Th2 differentiation. Th1 cells produce IL-2 and interferonγ (IFN-γ) to maintain cell mediated immunity against intracellular organisms such as viruses and mycobacteria, and Th2 cells produce IL-4 and IL-13 promoting the differentiation of B cells to plasma cells and the induction of class-switching resulting in IgE production. Differentiated plasma cells produce immunoglobulins which participate in mucosal defense against extracellular organisms including H. pylori. Groundbreaking research inspired subsequent studies which finally led to the discovery of Th17 cells [Steinman, 2007] and T regulatory cells (Treg) [Sakaguchi et al., 1995, 2008]. As a consequence of this pioneering research, T helper cells, at present, are sub-grouped into 4 types according to the differences in their cytokine productions (Table 1).

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Helicobacter pylori Suppresses Serum Immunoglobulin Levels in Smokers with Peptic Ulcer: Probable Interaction Between Smoking and H. pylori Infection in the Induction of Th1 Predominant Immune Response and Peptic Ulceration