2. • Several environmental antigens may stimulate an
adaptive immune response, immunologic memory
• These overreactions of the immune system to harmless
environmental antigens is called hypersensitivity
• This may produce tissue injury and other serious
diseases, often referred to as auto-immune diseases
• In other words hypersensitivity means that our immune
system reacts to something in such a way that it ends up
damaging itself instead of protecting it
3. • There are 4 types of hypersensitivity, based upon the
effector mechanisms by which they are produced-
4. • This type of hypersensitivity is mediated by antigen
specific effector T-cell
• The duration between exposure to antigen and the
response is about 48-72 hours, hence it is also referred
to as delayed type hypersensitivity
• In type-IV hypersensitivity, cytotoxic CD8 T-cells and
helper T-cells (CD4) leads immunogenic response
5. • Antigen is picked up antigen presenting cells(APCs) i.e.
dendritic cell or macrophages
• Carried to nearest lymph mode
• Where this APC present antigen using either MHC-II or
MHC-I receptor
6. • APC present antigen using MHC-II receptor, serving
platter for CD4 T-cell
• Th cell recognise antigen and binds to it using co-receptor
arm (CD4 arm)
• Th cell also produces CD28 protein that binds to B7
protein on the surface of APC
• APC releases IL-12 cytokines that matures Th cell into
Th1 cell
• Th1 cell relese IL-2 cytokines that helps in proliferation of
Th1 cells
• Also releases IFN that activates macrophages and
creates more Th1 cells
7. • Also macrophages releases cytokines like TNF, IL1, IL6
• These cytokines causes leakiness in endothelial barriers
and more immune cells are recruited, leading tp redness
edema, and sometimes fever
• Lysosomal enzymes, reactive oxygen species are also
produced that leads to tissue damage
8.
9. • Dermatitis- caused by poison ivy or by wearing iron or
nickel
• Apart from skin diseases, systemic diseases like multiple
sclerosis where Th1 cells damage myelin around nerve
fibre
• Tuberculin reaction- if person is exposed to tuberculosis
previously, Th1 cells migrate to reaction site and
inflammatory response, that makes skin thick and hard
10. • These are killer T-cells, these cells destroys cell directly
• APC present antigen on MHC-I molecule (present on
every nucleated cell)
• MHC-I molecule present antigen present inside the cell
• E.g.- Virus infected cells, cancerous cells
• After CD8 cell binds to antigen , CD8 cell releases
cytokines perforin and granzymes
• Perforin forms pores in cell membrane and granzymes
enters cell that induces apoptosis
11.
12. • Hashimoto thyroiditis- where CD8 cells attack thyroid
epithelial cells
• Type 1 Diabetes- CD8 cells target pancreatic -cells
Editor's Notes
Sometimes APC releases IL-6 and trasformin GF- and Th-17 cells are produced, these cells releases IL-17 that recruits neutrophils