DR. ROOPAM JAIN PROFESSOR & HEAD, DEPT. OF PATHOLOGY & BLOOD BANK

1. Diseases of
the Immune
System - 7
DR. ROOPAM JAIN
PROFESSOR & HEAD, DEPT. OF PATHOLOGY

2. Hypersensitivity:
Immunologically Mediated
Tissue Injury

3. • Injurious immune reactions, called hypersensitivity, are the
basis of the pathology associated with immunologic
diseases.
• Hypersensitivity reactions can be elicited by exogenous
environmental antigens (microbial and nonmicrobial) or
endogenous self antigens

4. • Hypersensitivity usually results from an imbalance between
the effector mechanisms of immune responses and the
control mechanisms that serve to normally limit such
responses.
• The development of hypersensitivity diseases (both allergic
and autoimmune) is often associated with the inheritance of
particular susceptibility genes.
• The mechanisms of tissue injury in hypersensitivity
reactions are the same as the effector mechanisms of
defense against infectious pathogens

5. Classification of
Hypersensitivity Diseases
• In immediate hypersensitivity (type I hypersensitivity)
• the injury is caused by TH2 cells, IgE antibodies, and mast cells
and other leukocytes.
• In antibody-mediated disorders (type II
hypersensitivity)
• secreted IgG and IgM antibodies injure cells by promoting their
phagocytosis or lysis and injure tissues by inducing
inflammation

6. Classification of
Hypersensitivity Diseases
• In immune complex–mediated disorders (type III
hypersensitivity)
• IgG and IgM antibodies bind antigens usually in the
circulation, and the antigen-antibody complexes deposit in
tissues and induce inflammation.
• The leukocytes that are recruited (neutrophils & monocytes)
produce tissue damage by release of lysosomal enzymes
and generation of toxic free radicals

7. Classification of
Hypersensitivity Diseases
• In cell-mediated immune disorders (type IV
hypersensitivity)
• sensitized T lymphocytes (TH1 and TH17 cells and CTLs) are
the cause of the tissue injury.

8. Mechanisms of
Hypersensitivity Reactions

9. Comparative features of 4 types
of hypersensitivity reactions.

10. Schematic
representation of
pathogenesis of 4
types of
immunological
tissue injury.

12. Sequence of events in
immediate (type I)
hypersensitivity.
Immediate hypersensitivity
reactions are initiated by the
introduction of an allergen, which
stimulates TH2 responses and IgE
production in genetically susceptible
individuals.
IgE binds to Fc receptors on mast
cells, and subsequent exposure to
the allergen activates the mast cells
to secrete the mediators that are
responsible for the pathologic
manifestations of immediate
hypersensitivity.

17. Immune complex
disease
The sequential phases in the
induction of systemic immune
complex–mediated diseases
(type III hypersensitivity)

20. AUTOIMMUNE
DISEASES

21. PATHOGENESIS (THEORIES) OF
AUTOIMMUNITY
• Th e mechanisms by which the immune tolerance of the
body is broken causes autoimmunity.
• These mechanisms or theories of autoimmunity may be
exogenous or endogenous, and include
• immunological,
• genetic, and
• microbial factors - e.g. EBV infection), and less often
bacteria (e.g. streptococci, Klebsiella) and mycoplasma,

22. Criteria for diagnosis of autoimmune diseases

23. TYPES AND EXAMPLES OF
AUTOIMMUNE DISEASES
• 1. Organ specific (Localised) diseases
• 2. Organ non-specific (Systemic) diseases

25. Autoimmune
diseases

26. Organ specific & systemic autoimmune
diseases

27. Autoantibodies in Systemic
Autoimmune Diseases

28. Systemic Lupus Erythematosus
(SLE)
• SLE is the classical example of systemic autoimmune or
collagen diseases.
• The disease derives its name ‘lupus’ from the Latin word
meaning ‘wolf’ since initially this disease was believed to
affect skin only and eat away skin like a wolf.
• 2 forms
• 1. Systemic or disseminated form
• 2. Discoid form

29. ETIOLOGY
• 1. The exact etiology of SLE is not known.
• 2. Genetic factors.
• 3. Environmental factors.
• i) certain drugs e.g. penicillamine D;
• ii) certain viral infections e.g. EBV infection; and
• iii) certain hormones e.g. oestrogen

30. PATHOGENESIS
• Interaction between susceptibility genes and environmental
factors results in abnormal immune responses by formation
of various autoantibodies.
• i) Antinuclear antibodies (ANA)
• ii) Antibodies to double-stranded (anti-dsDNA)
• iii) Anti-Smith antibodies (anti-Sm)
• iv) Other non-specific antibodies

31. Morphology of
major lesions
in SLE

32. Morphology of major lesions in SLE

33. Morphology of major lesions in SLE

34. Morphology of major lesions in SLE