Pathology of immune system презентация

with basis of law






Pathology of immune system








Lecture on pathological anatomy for the 3-rd year students

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

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

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.

immune
tolerance

It consists of 2 parts which are divided into lobules, each of which has a cortex and cerebral substance.

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.

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.

pancreas);
— Mammary glands.

MALT
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

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.

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

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
formation of normal immune complexes

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.

system

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.

hypersensitivity),




⮚Immune complex-mediated disorders
(type III hypersensitivity ),





⮚Cell-mediated immune disorders - slow type (type IV hypersensitivity ).

minutes after the connection of an AG with AB bound to mast cells in individuals previously sensitized to the antigen

amines and other mediators from mast cells; recruitment of inflammatory cells (late-phase reaction)

Immediate hypersensitivity (type I)

Pathologic lesions:
Vascular dilation, edema,

Smooth muscle contraction,

Mucus production,

Inflammation

the host has become sensitized

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:

(anaemia), edema, blisters, neurodermitis,

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).

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 .

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.

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:
transfusion reactions;
erythroblastosis fetalis (hemolytic disease of the newborn);
autoimmune hemolytic anemia, agranulocytosis, and thrombocytopenia, in which individuals produce
antibodies to their own blood cells, which are then destroyed;
certain drug reactions, in which antibodies are

produced that react with the drug.

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

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

eliciting inflammation at the sites of deposition.

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)

Inflammation

in the blood circulation and are deposited in many organs

localized in particular organs, such as:
kidneys (glomerulonephritis),

joints (arthritis),

small blood vessels of the skin

if the complexes are formed and
deposited locally.

of the immune complexes in various tissues, thus initiating


an inflammatory reaction at the

sites of immune complex deposition

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.

inflammatory reaction (third phase). Two mechanisms are believed to cause inflammation at the sites of deposition:

activation of the complement cascade,
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.

after AG administration), clinical features appear:

urticaria,

arthralgias,

lymph node enlargement,

proteinuria.

(sensitized) T-lymphocytes.
Mechanisms of T cell-mediated (type IV) reactions

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.

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.

cytokines and
macrophage activation;

Activation of T-cell-mediated cytotoxicity


Pathologic lesions:
Perivascular cellular infiltrates;
edema;
cell destruction;
granuloma formation