Hypersensitivity: Types

00:01 So we’re going to look at each of these four different types, and I’ll explain to you exactly what’s involved in these different types of hypersensitivity reaction.

00:11 So Type I - IgE mediated mast cell degranulation.

00:16 So here we have a mast cell, and on the surface of mast cells are Fc receptors that are specific for the IgE class of antibody.

00:26 This is in fact the high affinity IgE receptor that’s called FcεR1.

00:34 So this will bind IgE antibodies by the Fc region of the antibody.

00:39 That’s why it’s called an Fc receptor.

00:42 And we all have mast cells sitting in our tissues that have IgE on their cell surface.

00:48 And it doesn’t cause any problems at all.

00:50 The problem arises, is if an antigen comes in which the IgE is specific for, and that antigen binds to the IgE.

01:02 Because what happens then, is that the IgE antibodies on the surface of the mast cell get linked together; we use the term cross-linked.

01:10 And if this substance is a completely innocuous substance, for example grass pollen, we refer to it as an allergen.

01:19 It’s going to generate allergy.

01:24 And the consequence of the IgE antibodies being linked together by the allergen is that the mast cells release their granules, they degranulate.

01:42 Type II hypersensitivity is cytotoxic antibodies against cell surface antigen.

01:50 So here we have a cell surface, with some antigens present on the cell surface, and antibodies are bound to those antigens.

01:59 Sometimes the antibodies can be directly toxic to the cell.

02:05 However, in most cases, other components of the immune response are required in order for these antibodies to actually damage the cell.

02:15 So for example, the classical pathway of complement may become activated, leading to the production of the membrane attack complex.

02:25 Or killer cells, that is any cell that is able to participate in ADCC.

02:32 So this term K-cell is used as a generic description of cells able to participate in ADCC.

02:40 There’s only two things you need from a cell to do that.

02:43 You need it to have an Fc receptor, and you need it to be able to produce toxic molecules.

02:50 Or macrophages that again have Fc receptors on their surface and are able to attack the coated cell.

03:07 Type III hypersensitivity is immune complex mediated hypersensitivity.

03:12 Now, all that term means, immune complex, is simply an antibody bound to an antigen, and you know that’s what antibodies do isn’t it? They bind to antigens.

03:21 But in this situation, there is a binding to an inappropriate antigen or immune complexes are becoming trapped in small tissue spaces in the body and causing pathology.

03:33 So for example, macrophages can become activated, complement can become activated.

03:40 There will be recruitment of neutrophils if complement component C5a is generated, because that’s a very potent chemotactic factor for neutrophils, and pathology will ensue.

03:53 And then finally, Type IV hypersensitivity, delayed type hypersensitivity.

03:58 It’s called delayed type hypersensitivity because it takes a little while to get going.

04:02 The other three types, you can have antibody that's already present, and as soon as the antigen comes into the body, the response will happen immediately.

04:10 For T-cells, you need them to expand up in number, to proliferate, to differentiate, and to start secreting cytokines.

04:18 So typically, type IV hypersensitivity takes two or three days before you actually see any effects.

04:26 And there is recognition of peptide MHC Class II by the T-cell receptor on a T-cell that is going to mediate this hypersensitivity reaction, most commonly by producing excessive amounts of cytokines.