Lecture10.ppt

Immunology BE433 Dr Christine Loscher Lecture 10 Immunological Memory When the immune system fails. Cytokines important in direction of T helper cell response Th1 and Th2 cells cross-regulate each other Immunological memory • The ability of the immune system to respond more rapidly and effec...

Immunology BE433 Dr Christine Loscher Lecture 10 Immunological Memory When the immune system fails. Cytokines important in direction of T helper cell response Th1 and Th2 cells cross-regulate each other Immunological memory • The ability of the immune system to respond more rapidly and effectively to pathogens that have been encountered previously • Reflects the existence of a clonally expanded population of antigen-specific lymphocytes – population is small but persistent and highly specialised • Not the same as the primary response – especially in production of antibodies • Long lived Memory cells • Most are in a resting state • A small percentage are dividing at any one time • Cytokines such as IL-7 and IL-15 have been shown to maintain these cells • Higher numbers than previously present of naïve cells • Respond rapidly Memory B cell response – increase in number of cells and affinity of antibody produced Failure of Host Defence Mechanisms Pathogens can evade the immune system • Antigenic variation allows pathogens to escape our immune defences Some viruses persist by ceasing to replicate until immunity wanes/becomes poor • Some viruses enter a latent phase – herpes simplex • Virus does not cause disease but as it is not replicating it cannot be detected/eliminated by the immune system • Factors such as bacterial infection, light or hormones can activate the virus Some pathogens can use host defence mechaisms and exploit them for their survival • Mycoacterium tuberculosis (TB) lives in macrophages by preventing fusing of phagosome and lysosome • Treponema pallidum (syphilis) avoids recognition by antibodies by coating its surface with host molecules until it gets to the CNS where it is less easily reached by Ab • Other viruses can synthesis complement regulatory molecules – turn off complemet • Can inhibit MHC1 synthesis and assembly Immunodeficiency Diseases • When one or more components of the immune system is defective • Usually diagnosed following a history of repeated infection • Recurrent infection by pyogenic/pus-forming bacteria suggests a defect in antibody, complement or phagocyte function • History of fungal skin infections or recurrent viral infections suggests a defect in host defence mediated by T lymphocytes • Inherited disease caused by recessive gene defects Immunodeficiency • Low Ab levels results in failure to clear extracellular bacteria • T cell defects can also result in poor Ab levels • Defects in complement components cause defective humoral immune function • Defects in phagocytic cells permits widespread bacterial infection • Defective T cell signaling, cytokine production or cytokine action can cause immunodeficiency Human immunodeficiency syndrome (HIV) • Infects CD4 T cells, dendritc cells and macrophages • Genetic deficiency of the macrophage chemokine coreceptor for HIV confers resistance to HIV infection • Those with a mutant CCR5 have some degree of protection • Offers the possibility of a therapy • DNA integrates into the host genome • Transcritpion of HIV virus depends on host-cell transcription factors induced upon activation of infected T cells • Drugs that block HIV replication lead to rapid increase in CD4 cells and decrease in virus titre Allergy Allergy mediated by IgE Treatment of allergy