Immunology Notes

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Department
Microbiology and Immunology
Course
Microbiology and Immunology 3300B
Professor
Rodney Dekoter
Semester
Winter

Description
Immunology NotesNov 312 Humoral immunity means immunity due to proteins circulating in the blood such as antibodies in adaptive immunity or complement in innate immunity There is a beginning and end to an immune response First there is establishment of infection with the entry of the microorganism When numbers of the pathogen increase and exceed the threshold level of antigen required for an adaptive immune response the adaptive response is initiated The adaptive response doesnt get involved until the innate response cant contain the infection After 47 days effector cells and molecules of the adaptive response start to clear the infection When the infection has been cleared and the level of antigen falls below the response threshold the response ceases Antibody residual effector cells and immunological memory provide lasting protection against reinfection In the absence of innate immunity there is rapid growth of pathogen In mice or humans with SCID or Rag mutations the have innate immunity but dont have T or B lymphocytes and so lack adaptive immunity The duration of infection is much longer A nave T cell can interact with DC to become an activated but not committed Th0 cell Th0 can then become Tfh Th2 Th1 Th17 or Treg depending on what cytokines are expressed Th2 is involved in defence against parasites and allergy Th1 is involved in defence against intracellular pathogens Th17 is involved in defence against extracellular pathogens Treg is involved in immunosuppression The transcription factors involved commit the T cell to differentiate into a particular cell type Th17 vs Treg differentiation Treg cells are inhibitory Th17 cells are involved in defence against extracellular bacteria They are induced by TGF and IL6 and expanded by IL23 gives survival and proliferative signals These cytokines come from activated DCs Th17 cells make IL17 The expression of IL17 induces cells with the IL17 receptor to secrete IL6 involved in positive feedback CXCL8 and CXCL12 help recruit neutrophils and GMCSF and GCSF help with neutrophil and macrophage activation In the absence of infection DCs make mostly TGF and little IL6 CD4 T cells that encounter antigen will be induced to express FoxP3 and become Treg cells Treg cells can inhibit Th1 and Th2 cells Infection by pathogen induces DCs to produce high IL6 and IL23 Nave T cells will express transcription factor RORt and become Th17 cells Cytokines produced by Th17 cells IL17 induce cells such as epithelium to secrete chemokines that attract inflammatory cells such as neutrophils Th1 differentiation Th1 cells are involved in defence against intracellular pathogens They are induced by IFN which comes from NK NKT and CD8 T cellsrecognize infection innately They are expanded by IL12 which comes from DCs and macrophages TLR signalling and activation is important in driving DCs to produce IL12 Th1 cells secrete IFN and the transcriptional factor Tbet Viruses and bacteria induce IL12 secretion by DCs that can activate NK cells to produce IFN Nave CD4 T cells activated in the presence of IL12 and IFN are committed to differentiate into Th1 cells Effector mechanisms of Th1 cells Activation of CD8 T cells activation of phagocyte killing mechanisms and class switch to IgG2 and IgG3 The cytokines IL12 and IL23 share a p40 subunit and their receptors share the IL12R1 subunit IL12 activates the transcriptional factor STAT4 which increases IFN production Both cytokines augment the activity and proliferation of the CD4 subsets that express receptors for them Th1 cells express IL12 and Th17 cells express IL23 Th2 differentiation Th2 cells are involved in defence against extracellular parasites and allergy They are induced by IL4 which comes from iNKT mast cells basophils Th2 T cells They express IL4 and transcriptional factor GATA3 Pathogens cause the secretion of IL4 from these different cell types Nave CD4 T cells activated in the presence of IL4 are committed to differentiate into Th2 cells Effector mechanisms of Th2 cells Drive class switch to IgE and IgG1
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