Hypersensitivity reactions| type 1, type 2, type 3 and type 4 hypersensitivity

By Adem Lewis / in , , , , , , , , , , , , , , , , , , , , , , , , /

Immediate (type 1) hypersensitivity: Th2-mediated
diseases These disorders are characterized by abnormally
strong Th2 responses against environmental antigens that are essentially ignored by the
~75-80% of the population that does not suffer from allergies. All the clinical and pathologic manifestations
of allergy are the result of cytokines produced by Th2 cells (Fig. 2). IL-4 stimulates B cells specific for the antigens
to produce IgE antibody, which then binds to mast cells. When the antigen binds to this antibody, it
activates mast cells to release many mediators (histamine, proteases,
cytokines) that cause the acute vascular and smooth muscle reactions and inflammation that
are typical of allergies. IL-5 made by Th2 cells activates eosinophils,
which can exacerbate tissue damage. Th2 cells also secrete IL-13, which acts on
mucosal epithelial cells to stimulate secretion of mucus. Bronchial asthma is a Th2-mediated disease
about which you will hear more in the �Organs� block. The propensity to develop allergies is genetic,
but the actual genes that may be causative have not been definitively identified. How antibodies damage tissues: types 2 and
3 hypersensitivity Antibodies other than IgE can cause severe
tissue injury. In some cases, antibodies may be produced
against cell or tissue antigens and may deposit on cells or in the tissues (antibody-mediated,
or type II, hypersensitivity). Usually, these are autoantibodies, and their
production reflects a failure of self-tolerance. In other cases, antibodies against self-antigens
or microbial antigens may form immune complexes if the antigens are present in the circulation,
and these complexes may deposit in vascular walls (immune complex-mediated, or type III,
hypersensitivity). The �tail� of the antibody activates a
series of plasma proteins that make up the are activated by microbes or by antibodies
bound to microbes and tissue antigens, and are deposited on these surfaces. Various products of complement bring in leukocytes
(inflammation); are recognized by phagocytes, resulting in phagocytosis of coated cells;
and promote death of cells on which complement proteins are deposited. The tail of the antibody (called the Fc piece
because this fragment has a propensity to and neutrophils). Once these pathways are activated, they cause
disease in several ways (see Fig. 4). A. If the antibody is deposited on a cell
(e.g. erythrocyte or platelet), the combined action of complement and Fc receptors results
in that cell being eaten and destroyed by phagocytes. (This is the basis of red blood cell and platelet
depletion in autoimmune hemolytic anemia and thrombocytopenia, respectively.) B. If the antibody is deposited on a solid surface
the phagocytes may be activated and release toxic substances that induce inflammation
and damage the tissue (as in some forms of glomerulonephritis). C. Less commonly, antibodies can cause disease
by interfering with normal molecules (such as hormones and hormone receptors), without
any actual tissue injury; examples include myasthenia gravis (BMB) and Graves� disease
(M&N). F. How T lymphocytes damage tissues: type
4 hypersensitivity T lymphocytes injure tissues by two principal
mechanisms (Fig. 4). 1. CD4+ T lymphocytes of the Th1 subset produce
cytokines that activate macrophages (mainly IFN-?) and
recruit inflammatory cells (TNF). Th17 cells secrete cytokines that also recruit
leukocytes, such as neutrophils, and may
thus be major contributors to inflammation in T
cell-mediated hypersensitivity disorders. These reactions are called Delayed type hypersensitivity,
because they take 24-48 hours t develop after antigen challenge (the classical example is
a PPD skin test). Th1 and/or Th17 reactions against self-antigens
or against persistent microbes are responsible for many chronic disorders that you will hear
about (Crohn�s disease, type-1 diabetes, multiple sclerosis, rheumatoid arthritis). 2. CD8+ CTLs directly kill host cells, as in viral hepatitis (mentioned above). CTL-mediated cell injury may also contribute
to some Th1-mediated disease such as type-1 diabetes.

68 thoughts on “Hypersensitivity reactions| type 1, type 2, type 3 and type 4 hypersensitivity

  1. Thanks for great video ! I have a question about this type of immunoglobulin on surface of B cell when react with TH cell in Type I hypersenesitiviy reactions. Thanks

  2. was really confused n scared after seeing slides and hypersensitivity pages in kuby. but i was sure u could make it easy for me.. my practicals and immunology theory i totally dedicate to u sir keep going its really worthy and helpful thnx alot 🙂

  3. These are wonderful pieces of wOrk sir . thank you for wonderful efforts . I can't be grateful enough .

  4. Sir you already have made Immunology videos covering most of the topics previously in 2013? So sir which video series should i refer to the earlier ones or the 2016 videos?? Plz do reply my exams are very near and as always your lectures are my saviour.

  5. Isn't it auto immunity when the body recognises self as non self? Hypersensitivity could still be due to external factors like food, antibiotics and bacteria right?

  6. Lots of missing details. No mention of the antigen presenting cell role, TH cells to TH2 cell transformation, IL4/13 cytokines, and co-stimulation of CD4 and B cells in Type I IgE class switching. I can't seem to find a decent video on this stuff and the textbook (Janeway) is not the clearest either.

  7. Thank u very much sir fr tis nice video. You don't know how much u helped me! Now I have started to love my subjects cuz of u.

  8. Thanks so much sir
    ..i was trying from past 2 days to understand it from book ..i just wasted my time ..after watching 2 times this video ..i have no need to see the book now ..i can write direct in the exam thanks

  9. U r like magician to students like us🤗I think no one other can explain things and make it easier like u….. heartily nd extremely THANKFUL to u for all yr videos

  10. Ty sooo much sir ur videos are very help full ,i'm just going through ur videos keeping all my books aside ,keep doing sir

  11. sir u said dose are allergens … but i m lil confused for type 3 u gave rheumotoid arthiritis example may i knw d allergen for it??? exactly wats d allergen for it??

  12. Your the best one in every thing Ido not know How to thank you sir Iwish to be in good health and thank you very much god bless you

  13. It's vry hard to understand foreign authors book …i just start confusing when i saw many slides about hypersensitivity … but know im very clear in this topic because you just convey the idea very clearly and in a easy manner….thank you sirrr…please keep doing more videos for us sir

  14. please make video on please


    1) General introduction,

    2) infection,

    3) factors influencing


    4) kinds of immunity,

    5) vaccines

    6) (i.e. Tetanus vaccine,

    7) Diptheria vaccine,

    8) BCG vaccine,

    9) small pox vaccine),

    10) virus immunity,

    11) toxoids,

    12) toxins,

    13) daignostic preparation,

    14) sera,

    15) antitoxins

    16) (i.e. Diptheria


    17) Botulinium antitoxins),

    18) brief control of

    immunological products-

    19) Identification tests,

    20) toxicity tests,

    21) sterility tests,

    22) potency tests and

    23) storage of

    immunological products.

  15. Thank you so so much for this video ! I was struggling so much with this, but in 20 min you explained it waaaayyy better than my professor did in 6 months. Keep up the amazing work <3

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