IMMUNOLOGY AND HOST DEFENCES
The human body is made of 100 trillion cells of which 80 trillion are bacteria and viruses. "So are we the
host for the bacteria or is it the other way round"? asks Prof Dr. M. L. Kothari from KEMH Bombay India. whether bacteria cause tissue necrosis or whether it is the body’s over reactive WBC which launches an immune
attack on the cells in response to the presence of bacteria, MLK asks .
An infection usually
steps up the body temperature via cytokines and prostaglandin’s released by WBC's to boost the immune responses causing
fever , increases the heart rate and cardiac output to increase the blood flow, stimulates the marrow to increase production
of leucocytes, generates immunoglobin’s specific to the bacterial strain as well as memory cells to remember the antigenic
structures and increases the cortisone to enhance repair as well as causes heptosplenomegaly where increased destruction of
bacterial antigen can occur.
Basic physiology is elaborated
upon NOW, as this forms the cornerstone on which rests the body’s defence system
( against infection )
(A) INNATE IMMUNITY
in stomach destroys swallowed organisms .
in respiratory tract, urinary tract, etc.
( 20 protein enzyme) system in blood destroy bacteria.
Lysozymes ( a carbohydrate )
in blood destroys bacteria.
d. Neutrophils ( phagocytic ) and lymphocytes ( natural killer type ) destroys foreign
cells , tumour
cells , bacterial and viral cells.
(B) ACQUIRED IMMUNITY .
IMMUNITY - via immunoglobins produced by Beta- Lymphocytes.
MEDIATED - via direct attack by T- lymphocytes .
OF CELLS - involved.
Mast cells play a big role in Allergies and a small role in inflammation.
Their function is release of Heparin to keep circulatory blood liquid.
" THE IMMUNE RESPONSE "
In response to tissue insult by trauma, organisms, toxins, or autoimmune mechanism.
A) IMMEDIATELY a few local tissue macrophages start phagocytosis in the affected
tissue, local lymph nodes and the spleen , releasing –
(TNF) Tumour Necrosis factor which causes
increased blood flow , increased capillary
permeability to enable blood polymorphs to migrate onto the interstitial tissues.
Colony Stimulating factor and IL- l ( Interleukin- 1) and Ag (antigen) is released from the macrophage phagocytosis.
B) Within one hour , the migrated polymorphs begin phagocytosis.
C) Within 8 hours the few monocytes in circulation reach the tissue, mature into macrophages and begin phagocytosis. Though
few, they have 5 times the phagocytosis ability of neutrophils.
D) Within 3 - 4 days the CSF stimulates the bone marrow to increase polymorphs and monocytes which then reach the site.
E) Within several days of first days of first exposure the antigens stimulates the B- lymphocyte and T- helper cells to
release Interleukins which activate plasma cells to form B- lymphocyte clones. Upto 2000 immunoglobins are released per plasma
cell.Secondary response is 10-50 times the magnitude of the primary resonse.
a) IgM is released as a primary response to antigen on first exposure and
IgG is released as a secondary response to
antigen on second exposure
( IgM shows active infection )
IgE is present on mast cells.
IgA is present in secretions and mucosa.[ innate
natural immunity ]
IgD on the surface of B- lymphocyte.[natural
– blood ]
b) On second exposure
immmunoglobins are formed (IgG) immediately due to memory B- lymphocytes which form after first primary exposure which are
stored for many months or years. At any given time there are one million types
of memory cells in the blood.
Immunoglobins act via the series of enzymes 20 glycoproteins in the plasma called complement.to destroy
F) After several days , pus is formed which is either absorbed or let out through an outlet.
G) Tissue repair occurs
a) new cells are formed by multiplication of parenchymal cells.- regeneration , wherever possible
b) Fibroblast lay down fibrous tissue after stimulation by FGF ( Fibroblast Growth Factor ) released
by vascular endothelial cells wherever parenchymal regenerartion cannot compensate to maintain integrity and strengthen the
repaired tissue.- scarring
H) Cortisone is
released to nearly five- fold its usual value by the Adrenal Cortex
which inhibits excessive inflammatory response
tp prevent tissue injury.
Promotes tissue repair.
I)Mast cells release
histamine, bradykinin, serotonin, prostaglandins complement and clotting factors and play a large role in dealing with allergic inflammatory release.
J)Cell Mediated Immunity is a response to viruses , mycobacteria, protozoan and tumor cells is via stimulation
of T- cells by the antigen, & is a secondary response, due to memory cells.
1. T- helper cells release lymphokines (cytokines) called
b) Interferon - destroy viruses.
2. T - inducer cells release Interleukines which help in antibody formation.
3. Cytotoxic T - cells.
Cytotoxic T - cells release perforins which perforate the cell-
destroy virus and cancer cells.
4. Supressor T- cells supress excessive immune responses.- regulate
In HIV for e.g. - It takes up to 10 years for full blown aids to develop because of body immunity.
a) Anti HIV . Antibody develop as humoral immunity.
b) CD4+ and CD8+ T - Lymphocytes develop as CMI which
supress HIV infection by the cytokines called ' RANTES'
c) NK ( Natural Killer T cells ) kill organisms or tumor cells .
Both types of immunity act together in
varying proportions during different types of insult.
SUMMARY OF INFLAMMATORY RESPONSE