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NAJRAN UNIVERSITY College of Medicine

NAJRAN UNIVERSITY College of Medicine. Microbiology &Immunology Course Lecture No. 16. By. Dr. Ahmed Morad Asaad Associate Professor of Microbiology. Cell mediated immunity

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NAJRAN UNIVERSITY College of Medicine

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  1. NAJRAN UNIVERSITY College of Medicine Microbiology &Immunology Course Lecture No. 16 By Dr. Ahmed MoradAsaad Associate Professor of Microbiology

  2. Cell mediated immunity • The cell mediated immunity (CMI) reactions are found to be responsible for a wide variety of protective mechanisms, e.g.: • - Resistance to many infectious agents especially intracellular pathogens, e.g. viruses,M. tuberculosis, M. leprae,brucella, listeria and salmonella. • - Resistance to fungal and protozoa infections. • - Resistance to tumours.

  3. Migration of immune cells and antigen recognition • B and T cells are in continuous migratory journey between blood and the lymphoid organs (lymph nodes, tonsillitis and spleen). • In the blood they may be accidentally stimulated by the circulating APC. • The lymphoid organs are populated by APC which entrap the microbes as B cells and macrophages. • This migratory movement is under the effect of certain receptors on B and T cells as selectin, integrin and Ig adhesion molecules.

  4. Characters of CMI • ‑ The cellular immune response is principally mediated by subclasses of T‑lymphocytes and macrophages.­ • ‑ On recognition of antigen, TH lymphocytes are activated: • They produce soluble mediators called lymphokines • Lymphokines attract monocytes, macrophages and lymphocytes to the site of the reaction. • Attracted cells are activated and stimulated to proliferate. • Activated macrophages kill intracellular microorganisms. • On the other hand, activated Fc lymphocytes directly kill virus‑infected cells, tumour cells and graft cells.

  5. STAGES OF CM1 RESPONSE 1. Antigen processing and presentation: ‑ The antigen presenting cells APC (principally macrophages and B cells) bind, ingest and digest protein antigens into peptide fragments. ‑ These are presented on the cell surface where they can be recognized by TH cells.

  6. 2. Activation of TH cells: • ‑ These are activated by 2 signals: • The first signal is recognition of the antigen presented on the surface of APC. • The second signal is interleukin‑1 (IL‑1), which is secreted by the activated macrophages.

  7. ‑ Activated TH cells secrete several lymphokines including interleukin‑2 (IL­2), which stimulates TH cells to proliferate into a clone of antigen specific TH cells. ‑ A proportion of these cells become effector cells releasing lymphokines(i.e. cytokines) and the remainder become memory cells, which provide secondary immune response. ‑ Gamma interferon ( IFN), one of the released lymphokines, activates macrophages and enables them to kill intracellular organisms. ‑ Other lymphokines stimulate infiltration and proliferation of inflammatory cells.

  8. 3.Activation of Tc cells: These also require 2 signals: ‑The first is the recognition of antigen on the surface of target cells, e.g. virus infected cells. ‑The second is lymphokines produced by activated TH cells, specially IL‑2, which activates Tc cells, stimulates them to proliferate and form a clone of cells, which kill target cells. 4.Activation of Ts cells: ‑Signals for activation are not known. ‑Ts cells regulate both the humoral and CMI response.

  9. The cellular interactions in the specific immune response.

  10. Effect of Superantigens on T Cells Superantigens are a class of bacterial toxins and retroviral proteins that have the ability to bind specific T-cell receptor (TCR). In so doing, they act as a "clamp" between them, providing signals to the T cells.

  11. Differences between Superantigens and Classical Antigens • - Superantigensare not processed by antigen presenting cells. • - Exposure to a superantigen, therefore, can lead to massive T‑cell activation and the release of large amounts of cytokines, especially, TNF, IL‑1, IL‑2 and IL‑6, which mediate the clinical effects of toxic shock syndrome such as fever, erythematous rash, emesis, hypotension, tissue injury and shock. • - No memory cells.

  12. Examples of Superantigens • 1- Staphylococcaltoxic shock syndrome toxin (TSST‑1) and its enterotoxins. • 2- Pyrogenicexotoxin A of Strept. pyogenes. • 3- Endotoxinsof gram negative bacteria. • 4- Retroviralproteins.

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