Last update:
13-Nov-2007

The immune system reacts to protect the host from infection. During the past 50 years immunologists have elucidated the basic mechanisms which control the immune response against pathogens. They have suggested theoretical models to explain patterns of immune recognition and response to infection. Some confirmed the theoretical aspects with critical experimental data contributing significantly to the field of the immunology of infectious diseases. In this review the initial self-nonself discrimination models (SNSD models) and Janeway's extended self-nonself model (infectious-non self discrimination model) are discussed. Janeway's theory underlined the critical role of innate immunity in infection. Janeway suggested that the immune system evolved to discriminate infectious non self from non infectious self. This model hypothesized that immune responses could not occur unless antigen-presenting cells were first activated, and they were activated via pattern recognition receptors (PRRs) that recognized evolutionarily conserved molecules on infectious non self organisms (pathogen-associated molecular patterns, PAMPs). Toll-like receptors are the most representative members of the PRRs family and they link functionally innate and adaptive immunity in infection. Innate immunity triggers and determines the type (T1, T2) of the adaptive immune response against pathogens. Recently Matzinger proposed the danger theory to answer those questions that classical SNSD models do not. The danger model suggests that the immune system is more concerned with tissue damage than with foreign invaders, and the PRRs are triggered by distressed tissue-derived danger/alarm signals. The hydrophobicity model proposed that the hydrophobic portions of biological molecules act, when exposed, as universal damage-associated molecular patterns to initiate repair, remodelling and immunity. Other theories concerning the recognition of the pathogen and the initiation and the outcome of the immune response, such as the integrity model and ignorance hypothesis, are also mentioned.

Key words: Immune response, Immunity, Infection, Models, Recognition.