Transcript Types of immune responses

Immunologic Inflammation
Datsko T.V.
Immunologic Inflammation
B Cell
The morphology of immunologically induced
inflammation depends on the initiating
antigen and the reacting component of the
immune system. Type I B-cell immune
reaction (allergy type) is characterized by
increased vascular permeability with edema,
platelet aggregation, and infiltration by
eosinophils (e.g., allergic rhinitis, asthma
bronchiale).
Immunologic Inflammation
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Type II B-cell reaction causes
lysis of the antigenic target cell or necrosis of
tissue components (e.g., autoimmune
hemolytic anemia, nephrotoxic glomerulonephritis). Type III B-cell immune
reactions or immune complex reactions are
characterized by accumulations of antigenantibody complexes and in situ complement
activation with subsequent serofibrinous
exudates; thickening of basement
membranes;
Immunologic Inflammation
and slow, secondary development of
granulation tissue at the site of immune
complex deposition (e.g.,
membranoproliferative
glomerulonephritis, certain lesions in lupus
erythematosus, and
rheumatoid arthritis). More acute reactions
cause acute vasculitis with or without
microhemorrhage (Arthus-type reaction).

Hypersensitivity
of
first
(immediate) type develop with the
participation of mast cells and
blood basophils. They produce IgE
when antigen (allergen) introduce
into organism.
Hypersensitivity of first (immediate) type
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Immune response to the action of antigen are formed
by lymphoid system of the body. It characterizes by:
a) specificity (valid for specific antigen);
b) potentiation (strengthening at the second introduction
of antigen);
c) immunological memory (recognizes antigen through a
long period of time between introductions).
The phases of the immune response:
presentation by macrophages through absorb
(phagocytosis);
antigen recognition by lymphocytes;
transformation;
T-and B-lymphocytes proliferation.
Types of immune responses:
- Primary;
- Secondary.
Immune response to the antigen action
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Immune response to the action of antigen are formed by
lymphoid system of the body. It characterizes by:
a) specificity (valid for specific antigen);
b) potentiation (strengthening at the second introduction of
antigen);
c) immunological memory (recognizes antigen through a long
period of time between introductions).
The phases of the immune response:
presentation by macrophages through absorb (phagocytosis);
antigen recognition by lymphocytes;
transformation;
T-and B-lymphocytes proliferation.
Types of immune responses:
- Primary;
- Secondary.
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Hypersensitivity of first (immediate) type

These reactions are
manifested with eczema,
dermatitis, allergic rhinitis
and gastroenteritis, atonic
asthma - local
manifestations.

Anaphylactic reactions
and shock - systemic
manifestations.
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
Hypersensitivity
of
second
type
(antibody-mediated hypersensitivity)
develops when interacting antibodies
(IgG or IgM) with the antigen on the
surface of cell with subsequent
(наступним) damage due to lysis,
phagocytosis by macrophages, cell
cytotoxicity by T-cell lymphocytes,
change cell function (neutralization or
hyperaction)
Hypersensitivity of second type (type II)
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Type I (allergic) reaction,
bronchial asthma with
prominent bullous emphysema
of the lung
Type II (toxic) reaction, necrotizing
glomerulus and vasculitis with
fibrinoid necrosis in patient with
panarteritis nodosa,
Immunologic Inflammation
Type II (toxic) reaction,
necrotizing glomerulus
and vasculitis with
fibrinoid necrosis in
patient with panarteritis
nodosa,
microscopic features
note the homogeneous
red necroses of
glomerular vessels and
arteries
Type I (allergic) reaction, bronchial asthma with prominent bullous
emphysema of the lung , and typical eosinophilic bronchitis with
sclerosis of epithelial
Type III (immune complex) reaction, membranous glomerulus with
immune complex deposits
Type III (immune complex) reaction,
membranous glomerulus with immune
complex deposits
microscopic features note the
prominent thickening of glomerular
capillary basement membranes .
Kidney transplant rejection (lymphocytic), gross appearance of
kidney (left), interstitial lymphocytic infiltration with tubular
damage (right, arrow).
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Gell and Coombs Type
Alias
Mechanism
Type I IR
Allergic IR Atopic IR Anaphylactic IR
Cytophilic antibodies (e.g., IgE) bind to mast cells; antigen
binding to these cell-bound antibodies causes mast cell
degranulation with release of vasoactive mediators (e.g.,
histamine), which initiate the microvascular inflammatory
response (thrombocytes and eosinophils cooperate).
Type II IR
Toxic or cytotoxic IR
Complement-binding antibodies (on antigen binding) activate
complement cascade, members of which initiate
inflammatory response by activating cell chemotaxis and
phagocytosis, ultimately causing toxic ceil and tissue
damage.
Type III IR
Immunocomplex IR
Persistence of antigen-antibody complexes are recognized
by the immune system as foreign and induce the production
of secondary anticomplex antibodies (i.e., anti-antibodies,
such as rheumatoid factor); these bind and activate
complement and cause tissue lesion through complement
components (see above).
Cell-mediated IR T-cell cytotoxic IR CTL
response
a. Direct destruction of target antigenic cells by binding of
CTL, Fas-related induction of apoptosis, and/or release of
perforin and granzymes
b. T-cell cytokine response activation of macrophages:
granulomatous (e.g., IFN-γ, TNF) reaction
c. T-cell cytokine response activation of mast cells: basophil
reaction (e.g., IL-3, IL-5)
d. T-cell cytokine response: activation of vasoproliferative
factors (e.g., IL-3, IL-8)
B-celi reactions
T-cell reactions
Type IV IR
Granulomatous pneumonitis showing gross (left) and
microscopic (right) features of pulmonary tuberculosis; note
the well-circumscribed granulomas with giant cells and central
(caseous) necrosis .
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Basophil reaction of skin following recluse
spider bites (left), microscopy of dermal
vessels (right).
Reaction of transplants rejection
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Autoimmune disease a manifestation of the damage of
natural tolerance of the immune
system to its own antigens.
This
tolerance is formed in the embryonic
period yet.
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Autoimmune diseases
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Autoimmune diseases can be:
 - Organospecific (Hashimoto
thyroiditis, insulinresistant
diabetes mellitus, multiple
sclerosis, encephalomyelitis,
polyneuritis, aspermatogeny
and others);
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- Organononspecific or
systemic disease (systemic
lupus erythematosus,
rheumatoid arthritis,
dermatomyositis, and
others).
Autoimmune diseases
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Autoimmune disease a manifestation of the damage of
natural tolerance of the immune
system to its own antigens.
This
tolerance is formed in the embryonic
period yet.

Autoimmune diseases
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Rheumatoid Arthritis
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Rheumatoid
synovitis
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Complications of Rheumatoid
Arthritis
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occurs when blood
incompatibility
of
mother and fetus
mainly through Rh
factor (the mother
"Rh-" fetus "Rh+"),
which
leads
to
hemolysis of fetal
red blood cells by
mother’s antibody.
Haemolytic disease
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Mother’s anamnesis:
ІІІ pregnancy, ІІ delivery
І pregnancy (1999) – healthy baby,
ІІ pregnancy (2002) – died down.
Mother has ІІІ Rh (-), titre of
аntibodies 1:64;
Caesarean section; 37-38 weeks,
valuation by Apgar scale 7/8 balls, Mass 2550; Child АВ (ІV) Rh (+);
Bilirubin from umbilical cord – 62,1; through 7 hours - 101,3 mkmoll/l;
through 13 hours - 133,6 mkmoll/l
1st day of life - with signs of intestinal obstruction,
Haemolytic disease of new-born shift into department of
Intensive therapy of neonates; perforation and peritonitis
developed through intestinal impassability of ІV degrees;
After 22 days - the child died.
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Complications of Rheumatoid
Arthritis
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Thank you for
attention !
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