Get information about immune system and its mechanism with detail.

1. Pathology of
immune
system

2. Functions of immune system
1. To provide defense of organism from:
-any infection,
-cells-mutants,
-tumor cells,
-transplanted cells,
-any substances which are recognized
by IS as foreign.
2. Permanent control by lymphocytes of
AG composition of own cells in
accordance to the HLA type 1 or 2

3. Organs of IS:Organs of IS:
Central organs:
bone marrow and thymus
There is a permanent rhythmic new
formation of immune cells not
depending on immune (AG)
stimulation of organism
Peripheral organs:
lymphatic nodules, spleen, mucosa-
associated lymphoid tissue
Additional reproduction and AG-related
differentiation of immune cells takes place
there in reply on the AG-stimulation

4. Bone marrowBone marrow
1. Active (red) bone marrow consists of
lymphopoetic cells, fatty tissue, vessels
and fibroblasts. At adults it is situated in
a breastbone, bodies of vertebrae, ribs
and pelvic bones.
2. Yellow bone marrow can transform into red
if it is necessary.
After 70 years old the atrophy of myeloid
tissue is seen, it is consists of fatty tissue and
fibrocytes.
 Children have active marrow in the
tubular bones, but after children
became grown up it change into yellow.

5. ThymusThymus
3-types of Т-lymphocytes
are produced in Thymus:
Т-killer
Т-helper, NK-cells
T-suppressors - they stimulate immune
tolerance
It consists of 2 parts which are
divided into lobules, each of
which has a cortex and cerebral
substance.

6. LYMPHATICLYMPHATIC NODULESNODULES
Control and AG recognition is provided in a lymph:
 Size of lymphatic nodules: 3-30мм.
 Lymphatic nodules
consists of: - cortex
- medullar substances
In cortex there are lymphatic follicles
(primary and secondary – with the center of
reproduction
–B-cells are formed there (B-zone)
In cerebral substances there are veins and
lymphatic sinuses.

7. SPLEENSPLEEN
Control and the AG-recognition of blood.
Every artery is surrounded by lymphatic
follicles. Red pulp is a potential active
mesenchymal tissue (there are B-lymphocytes)
Mass =150-180 gr.
A spleen can deposit up to the 2/3 of vein blood
volume.
In pathology it is an organ of extra-medullar
blood-formation.

8. (in the peribronchial fascial sheath);
— Exocrine glands (salivary glands and
pancreas);
— Mammary glands.
MALTMALT
Mucosa-associated lymphoid tissue includes the
following structures:
— Lymphatic pharyngeal ring with the
pharyngeal, lingual, and palatine tonsils;
— Gut-associated lymphoid tissue (the follicles
of the duodenum, appendix, colon);
— Bronchi-associated lymphoid tissue

9. COMMON IMMUNE PROCESSES
Participants:
immunocytes
(Т and B-lymphocytes,
monocytes, plasmocytes)
attracted cells, not immune
plasma-molecular elements

10. Immune mechanisms
1.Innate immunity (natural, or native) refers to
defense mechanisms that are present before
infection and have evolved to specifically
recognize microbes and protect organism
against infections. Innate immunity is the first
line of defense, because it is always ready of
innate immunity, providing protection against
inhaled microbes.
2.Adaptive immunity (acquired, or specific)
consists of mechanisms that are stimulated
by microbes and are
capable of also recognizing non-microbial
substances (AG). It consists of lymphocytes and
their products, including AB.

11. Adaptive immunity
There are two main types:
1.cell-mediated (or cellular) immunity, which is
responsible for defense against intracellular
microbes, it is mediated by T (thymus-derived)
lymphocytes
Performed by: - T-killer
- NK-cells
- macrophages
- labrocytes
- leucocytes (basophiles, neutrophils)
The result is formation of infiltrates and
granulomas, displays of immune cell killing
At final stage – phagocytosis and destruction of
intracellular bacteria and viruses, fungi, tumor
and transplanted cells

12. Adaptive immunity
2. Humoral immunity, which protects against extra-
cellular microbes and their toxins, it is mediated by B
(bone marrow-derived) lymphocytes
and their secreted products.
Performed by: - B-lymphocytes,
that transformed into plasmocytes
and produce Ig M, G, I
-activated complex of complement (C3 and C5)
At final stage: - lysis of bacterias and AG
-opsonisation and phagocytosis of bacteria
-destruction of immune complexes on basal
membranes
-neutralizations of exotoxins
-agglutinization of blood cells

13. TYPES OF IMMUNE ANSWER
Primary immune answer – arises up on
6-8 days after the first meeting with
AG; the AB titer is determined on 2-3d
week and is achieved a maximum
through 1 month, and then is gone
down.
 Secondary immune answer – arises up
through 2-3 days after meeting with AG,
the AB titer begins to determine on the
first week already, the AB is high during
one month and goes down during many
years.

14. Pathology of the immunePathology of the immune
systemsystem
Reactions of hypersensitiveness
Immunodeficiency syndromes
Autoimmune diseases
Amyloidosis
Tumors of the lymphatic system

15. Reaction of hypersensitivity
 The reaction of hypersensitivity is the
individual reaction on the repeated
reception of AG, which is exceeds the
measure of biological expedience on the
express and effect, because it is completed
by destruction of the cells and violation of
function.
 These reactions are unusual on the
methods of answer. The basis of these
reactions is a normal immune answer
which is perverted because of the unusual
reception or promoted reception of AG.

16. Types of reactions:Types of reactions:
Immediate hypersensitivity –
anaphylactic type (Type I),
Antibody-mediated disorders (Type II
hypersensitivity),
Immune complex-mediated disorders
(type III hypersensitivity ),
Cell-mediated immune disorders -
slow type (type IV hypersensitivity ).

17. Immediate hypersensitivityImmediate hypersensitivity
(Type I)(Type I)
It is a rapidly developing
immunologic reaction occurring
within minutes after the
connection of an AG with AB
bound to mast cells in individuals
previously sensitized to the
antigen

18. Immune mechanism is:
Production of IgE antibody ―immediate release
of vasoactive amines and other mediators from
mast cells; recruitment of inflammatory cells
(late-phase reaction)
Immediate hypersensitivityImmediate hypersensitivity
(type I)(type I)
Pathologic lesions:
Vascular dilation, edema,
Smooth muscle
contraction,
Mucus production,

19. 1.a systemic disorder - it follows injection of an AG to
which the host has become sensitized
2.a local reaction - the nature of reactions varies
depending on the entering of the AG
Systemic displays:
- spasm of respirator bronchiole (difficulty of
breathing) - acute respiratory insufficiency,
- respiratory D-stress syndrome (RDS),
- system disorders of haemodynamic and rapid
expansion of vessels – it leads to collapse with the
loss of consciousness and decreasing of arterial
pressure,
- gastroenteritis – it is spastically stomach-aches,
vomiting and diarrhea,
- allergens cause development of anaphylactic shock,
and medicinal allergens – anaphylactic reaction.
Immediate hypersensitivity (type I) may occur as:

20. Local displaysLocal displays
2.hay fever,
1.localized cutaneous swellings (skin allergy, hives)
- as hyperemia (anaemia), edema, blisters,
neurodermitis,
3. nasal and conjunctiva discharge (allergic rhinitis,
conjunctivitis and sinusopathy), can be seen at:
- inhalation of pollen of plants (polynosis), wool of
animals
- allergic edema of larynx after the appliqué of
medicines that leads to asphyxia.
4. allergic gastroenteritis (food allergy) - develops
on food allergens, the spasm of smooth muscle and
secretion of liquid in the road clearance of bowel is
seen (diarrhea).

21. 5.bronchial asthma - allergens cause the asthma
triad.
Morphology:
— Hypertrophic bronchial musculature is present as
a bronchial spasm sign.
— Hypersecretion of mucus: excessive mucus
production leads to mucus plugs formation and the
bronchial obstructions .
— Mucous membrane edema: eosinophilic infiltrate
in the mucous membrane leads to generation of
inflammation mediators, causing swelling of the
mucous membranes, and crystallization of
eosinophilic enzymes (Charcot-Leyden crystals .

22. АB-mediated hypersensitivity - type II
It is mediated by AB directed
toward AG present on cell surfaces
or extra-cellular matrix.
The antigenic determinants may be
intrinsic to the cell membrane or
matrix, or they may take the form
of an exogenous AG, such as a
drug metabolite, that is adsorbed
on a cell surface or matrix.

23. Mechanisms of AB-mediated reaction:
1. Opsonization and Phagocytosis
AB connects with AG at the cellꞌs surface (it is named opsonization).
This process is necessary for recognition the cell-target by
macrophages, with following destruction (phagocytosis).
Clinically it is occur as:
1.transfusion reactions;
2.erythroblastosis fetalis (hemolytic disease of the newborn);
3.autoimmune hemolytic anemia, agranulocytosis, and
thrombocytopenia, in which individuals produce
antibodies to their own blood cells, which are then destroyed;
4.certain drug reactions, in which antibodies are
produced that react with the drug.

24. 2. Complement- and Fc Receptor-Mediated
Inflammation.
The Fc portions of antibodies bonded to a foreign cell
or foreign material contact Fc-receptors on
macrophages, causing inflammation, cell injury and
death.
Mechanisms of AB-mediated reaction:
AB-mediated inflammation is the mechanism
responsible for tissue injury in some forms of
glomerulonephritis, vascular rejection in organ
grafts, and other diseases

25. 3. Antibody-Mediated Cellular Dysfunction
Mechanisms of AB-dependent reaction:
AB directed against cell-surface receptors impair or
dysregulate
function without causing cell injury or inflammation.
1.Myasthenia gravis - AB reactive with acetylcholine
receptors in the motor end-plates of skeletal muscles
impair neuromuscular transmission and therefore cause
muscle weakness.
2.In pemphigus vulgaris - AB against desmosomes
disrupt intercellular junctions in epidermis, leading to the
formation of skin vesicles.
3.In Graves disease - AB against the thyroid-stimulating
hormone receptor on thyroid epithelial cells stimulate the
cells, resulting in hyperthyroidism.

26. Immune complex-mediated
hypersensitivity - type III
Antigen-antibody complexes produce tissue
damage mainly by eliciting inflammation
at the sites of deposition.

27. Immune complex-mediatedImmune complex-mediated
hypersensitivityhypersensitivity –– type IIItype III
Immune mechanism is:
Deposition of antigen-antibody
complexes leads to complement activation
recruitment of leukocytes by complement
products and Fc-receptors release of
enzymes and other toxic molecules
Pathologic lesions:
Necrotizing vasculitis (fibrinoid
necrosis)

28. Types of iTypes of immmune complex-mune complex-
mediatedmediated
diseasesdiseases (type III)(type III)
1.generalized, if immune complexes are
formed in the blood circulation and are
deposited in many organs
2.localized in particular organs, such as:
- kidneys (glomerulonephritis),
- joints (arthritis),
- small blood vessels of the skin
if the complexes are formed and
deposited locally.

29. Phases of immune complex disease
1.formation of AG-AB complexes in
the blood circulation
2.deposition of the immune
complexes in various tissues, thus
initiating
3.an inflammatory reaction at the
sites of immune complex deposition

30. The first phase is initiated by the introduction of
AG, usually a protein, and its interaction with
immune-competent cells, resulting in the
formation of AB.
These AB are secreted into the blood, where
they react with the AG still present in the
circulation to form AG-AB complexes.
In the second phase, the circulating AG-AB
complexes are deposited in various tissues.

31. Once complexes are deposited in the tissues, theyOnce complexes are deposited in the tissues, they
initiate an acute inflammatory reaction (third phase).initiate an acute inflammatory reaction (third phase).
Two mechanisms are believed to causeTwo mechanisms are believed to cause inflammationinflammation
at the sites of deposition:at the sites of deposition:
1. activation of the complement cascade,
2. activation of neutrophils and macrophages.
Complement
activation promotes the migration of
polymorphonuclear leukocytes and
monocytes and inflammation. Thrombi are
formed in the vessels, resulting in local
ischemic injury.

32. Types of immune complex-mediated
diseases (type III)
During this phase
(approximately 10 days after
AG administration), clinical
features appear:
-urticaria,
-arthralgias,
-lymph node enlargement,

33. Cell-Mediated hypersensitivity (type IV) - slow
typeIt is initiated by AG-activated (sensitized)
T-lymphocytes.
Mechanisms of T cell-mediated (type IV)
reactions
1.The delayed type hypersensitivity reactions
mediated by CD4+ T-cells.
CD4+ T cells (and sometimes CD8+ cells)
respond to tissue AG by secreting cytokines that
stimulate inflammation and activate phagocytes,
leading to tissue injury.

34. Cell-Mediated hypersensitivity (type IV) - slow
type
It is the principal pattern of immunologic
response to:
-a variety of intracellular microbiologic
agents, such as Mycobacterium tuberculosis,
-viruses, fungis, protozoa, and simplest.
2. T-cell mediated cytolysis. CD8+ cytolytic
T-lymphocytes directly kill tissue cells.

35. Cell-Mediated hypersensitivityCell-Mediated hypersensitivity
(type IV)(type IV)
The immune mechanism of
activating T-lymphocytes leads
to:
1)Releasing of cytokines and
macrophage activation;
2)Activation of T-cell-mediated
cytotoxicity
Pathologic lesions:
 Perivascular cellular infiltrates;
 edema;
cell destruction;