Type IV Hypersensitivities Delayed Cell Mediated

Harmful effects produced by the mechanisms of cell-mediated immunity are referred to as delayed hypersensitivity. The name reflects the slowly developing response to antigen; reactions peak at 2 to 3 days rather than in minutes as in immediate hypersensitivity. As would be expected with cell-mediated responses, T cells are responsible and antibodies are not involved. Delayed hypersensitivity reactions can occur almost anywhere in the body. They are wholly or partly responsible for contact dermatitis (such as from poison ivy and poison oak), tissue damage in a variety of infectious diseases, rejection of tissue grafts, and some autoimmune diseases directed against antigens of self.

Tuberculin Skin Test

A familiar example of a delayed hypersensitivity reaction is the positive reaction to a tuberculin skin test that occurs in most people who have been infected with Mycobacterium tuberculosis. This test involves the introduction of very small quantities of protein antigens of the tubercle bacillus into the skin. In those with delayed hypersensitivity to M. tuberculosis, the site of injection reddens and gradually becomes indurated (thickened) within 6 to 24 hours. The reaction reaches its peak at 2 to 3 days (figure 18.6). There is no wheal formation, as would be seen with IgE-mediated reactions. The redness and induration of delayed skin hypersensitivity reactions are the result mainly of the reaction of sensitized T cells with specific antigen, followed by the release of cytokines and the influx of macrophages to the injection site.

Contact Hypersensitivities

Contact hypersensitivity is mediated by T cells. The T cells that have become sensitized to a particular antigen release

mm/id o

Figure 18.6 Positive Delayed (Type IV) Hypersensitivity Skin Test

Injection of tuberculin protein into the skin of a person sensitized to the tubercle bacilli causes a hardened red lump to form by 48 to 72 hours. A reaction greater than 10 mm in diameter is considered a positive reaction.

Nester-Anderson-Roberts: I III. Microorganisms and I 18. Immunologic Disorders I I © The McGraw-Hill

Microbiology, A Human Humans Companies, 2003

Perspective, Fourth Edition

450 Chapter 18 Immunologic Disorders

Carrier protein

Carrier protein

(b) Antigen-presenting cells (APC) present the hapten peptide complexed with MHCII to Th1 (inflammatory) CD4 T cells.

Exposure to poison oak

Exposure to poison oak

Hapten from the poison oak y Hapten peptide ' -

(b) Antigen-presenting cells (APC) present the hapten peptide complexed with MHCII to Th1 (inflammatory) CD4 T cells.

^ receptor

Was this article helpful?

0 0
Curing Eczema Naturally

Curing Eczema Naturally

Do You Suffer From the Itching, Redness and Scaling of Chronic Eczema? If so you are not ALONE! It strikes men and women young and old! It is not just

Get My Free Ebook

Post a comment