Helper T cells play a key role in cell-mediated immunity by activating other immune cells such as B cells and cytotoxic T cells. When a macrophage or dendritic cell engulfs and displays antigens from an invading pathogen on its surface, it activates matching helper T cells. Once activated, helper T cells secrete cytokines that stimulate B cells to produce antibodies and activate cytotoxic T cells to destroy infected cells. Both cell-mediated and antibody-mediated immunity then work together to eliminate pathogens from the body. Memory cells are also generated to facilitate a faster response upon future encounters with the same pathogen.

1. HEMATOLOGY
PART-II
PREPARED BY: JEGAN. S. NADAR

2. HEMOSTASIS
 HEMOSTASIS is the sequence of responses that stops bleeding
 Three mechanisms reduce blood loss:
 (1) Vascular Spasm,
 (2) Platelet Plug Formation
 (3) Blood Clotting (Coagulation).
Jegan

3. VASCULAR SPASM
When arteries or arterioles are damaged, the circularly arranged smooth muscle
in their walls contracts immediately
This reaction is called vascular spasm.
This reduces blood loss for several minutes to several hours, during which the
other hemostatic mechanisms go into operation
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4. PLATELET PLUG FORMATION
 Platelet plug formation occurs in following step
 Platelet adhesion
 Platelet release reaction
 Platelet Aggregation
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5. 1. Platelet Adhesion
Initially, platelets contact and stick to parts of a damaged blood vessel, such as
collagen fibers of the connective tissue underlying the damaged endothelial
cells.
 This process is called
platelet adhesion.
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6. 2. Platelet Release reaction
Due to adhesion, the platelets become activated.
They extend many projections that enable them to contact and interact with one
another.
They begin to liberate the contents of their vesicles.
This phase is called the platelet release reaction.
Liberated ADP and thromboxane A2 cause activation of nearby platelets.
Serotonin and thromboxane A2 function as vasoconstrictors.
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8. 3. Platelet Aggregation
 The release of ADP makes other platelets in the area sticky
 The stickiness cause newly recruited and activated platelets to adhere to the originally
activated platelets.
 This gathering of platelets is called platelet
aggregation.
 Eventually, the accumulation and attachment
of large numbers of platelets form a mass
called a platelet plug.
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9. BLOOD CLOTTING
 The process of gel formation is called clotting or coagulation which is a series of
chemical reactions that result in formation of fibrin threads
 Clotting involves several substances known as clotting (coagulation) factors.
 These factors include calcium ions (Ca2), several inactive enzymes that are synthesized
by hepatocytes or released by damaged tissues
 Clotting can be divided into three stages
 Formation of prothrombinase
 Prothrombinase converts prothrombin into thrombin
 Thrombin converts fibrinogen into fibrin
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11. THE EXTRINSIC PATHWAY
 The extrinsic pathway of blood clotting has fewer steps than the intrinsic pathway and
occurs rapidly
 It is so named because a tissue protein called tissue factor (TF), also known as
thromboplastin leaks into the blood from cells outside blood vessels and initiates the
formation of prothrombinase
 In the presence of Ca2, TF begins a sequence of reactions that ultimately activates
clotting factor X.
 Once factor X is activated, it combines with factor V in the presence of Ca2 to form the
active enzyme prothrombinase, completing the extrinsic pathway.
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13. THE INTRINSIC PATHWAY
 The intrinsic pathway of blood clotting is more complex than the extrinsic pathway.
 It occurs more slowly, usually requiring several minutes.
 The intrinsic pathway is so named because its activators are either in direct contact
with blood or contained within (intrinsic to) the blood
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14.  If endothelial cells become roughened or damaged, blood come in contact with
collagen fibers.
 In addition, trauma to endothelial cells causes damage to platelets, resulting in the
release of phospholipids by the platelets.
 Contact with collagen fibers activates clotting factor XII, which begins a sequence of
reactions that eventually activates clotting factor X.
 Once clotting factor X is activated, it combines with factor V to form the active enzyme
prothrombinase completing the intrinsic pathway.
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16. COMMON PATHWAY
 The formation of prothrombinase marks the beginning of the common pathway.
 In the second stage of blood clotting, prothrombinase and Ca2 catalyze the conversion
of prothrombin to thrombin.
 In the third stage, thrombin, in the presence of Ca2, converts fibrinogen, which is
soluble, to loose fibrin threads, which are insoluble.
 Thrombin also activates factor XIII (fibrin stabilizing factor), which strengthens and
stabilizes the fibrin threads into a sturdy clot.
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17.  Thrombin has two positive feedback effects.
 In the first positive feedback loop,
 It involves factor V, it accelerates the formation of prothrombinase.
 Prothrombinase in turn accelerates the production of more thrombin, and so on.
 In the second positive feedback loop
 Thrombin activates platelets, which reinforces their aggregation and the release of
platelet phospholipids.
Jegan

18. CLOT RETRACTION
 Once a clot is formed, it plugs the ruptured area of the blood vessel and thus stops
blood loss.
 Clot retraction is the consolidation or tightening of the fibrin clot.
 The fibrin threads attached to the damaged surfaces of the blood vessel gradually
contract as platelets pull on them.
 As the clot retracts, it pulls the edges of the damaged vessel closer together, decreasing
the risk of further damage.
 During retraction, some serum can escape between the fibrin threads, but the formed
elements in blood cannot.
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21. BLOOD GROUPS
 There are at least 24 blood groups
 More than 100 antigens that can be detected on the surface of red blood
cells.
 Two major blood groups—ABO and Rh system.
 Other blood groups include the Lewis, Kell, Kidd, and Duffy systems.
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22. ABO SYSTEM
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24. Rh SYSTEM
 The Rh blood group is so named because the Rh antigen, called Rh factor, was first
found in the blood of the Rhesus monkey.
 People whose RBCs have Rh antigens are designated Rh+ (Rh positive); those who lack
Rh antigens are designated Rh- (Rh negative).
 Normally, blood plasma does not contain anti-Rh antibodies.
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25. Rh SYSTEM
 If an Rh- person receives an Rh+ blood transfusion, however, the immune system starts
to make anti-Rh antibodies that will remain in the blood.
 If a second transfusion of Rh- blood is given later, the previously formed anti-Rh
antibodies will cause agglutination and hemolysis of the RBCs in the donated blood,
and a severe reaction may occur.
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27. TRANSFUSION
 A transfusion is the transfer of whole blood or blood components (red blood cells only
or blood plasma only) into the bloodstream or directly into the red bone marrow.
 In an incompatible blood transfusion, antibodies in the recipient’s plasma bind to the
antigens on the donated RBCs, which causes agglutination or clumping, of the RBCs.
 Agglutination is an antigen–antibody response in which RBCs become cross-linked to
one another
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28.  When these antigen–antibody complexes form, they activate plasma proteins of the
complement family
 In essence, complement molecules make the plasma membrane of the donated RBCs
leaky, causing hemolysis or rupture of the RBCs and the release of hemoglobin into
the blood plasma.
 The liberated hemoglobin may cause kidney damage by clogging the filtration
membranes
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29. IMMUNITY
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30. What is Immunity??
 It is the ability of an
organism to resist a
particular infection or
toxin by the action of
antibodies or white blood
cells
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31. IMMUNE SYSTEM
 INNATE
 ADAPTIVE
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32. INNATE IMMUNITY
 Innate immunity is nonspecific defense mechanisms that come into play
immediately or within hours of an antigen's appearance in the body.
 These mechanisms include
 Physical barriers such as Skin,
 Chemicals in the blood
 Immune system cells that attack foreign cells in the body.
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33. INNATE IMMUNITY
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34. First line of defence: External barrier
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36. Second Line of Defense: Internal Defenses
When pathogens penetrate the physical and chemical barriers of the skin and
mucous membranes, they encounter a second line of defense:
 Internal antimicrobial substances,
 Phagocytes,
 Natural killer cells,
 Inflammation,
 Fever.
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37. Antimicrobial Substances
 There are four main types of antimicrobial substances that discourage
microbial growth:
1. Interferons,
2. Complement system
3. Iron-binding proteins, and
4. Antimicrobial proteins.
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38. 1. INTERFERON
 Cells infected with viruses produce proteins called interferons or IFNs.
 Once released by virus-infected cells, IFNs diffuse to uninfected neighboring
cells.
 There they induce synthesis of antiviral proteins that interfere with viral
replication
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41. 2. COMPLIMENT SYSTEM
 A group of normally inactive proteins in blood plasma and on the plasma membranes
makes up the complement system.
 Bacterial cell wall made up of carbohydrate
 Complement protein attaches to specific carbohydrate chain on bacterial wall and leads
to formation of membrane attack complex
 Membrane attack complex are nothing but pores on the surface
 This cause the outside fluid to enter bacterial cell
 Because of this bacterial cell will burst (cytolysis)
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43. 3. IRON-BINDING PROTEINS
 Iron-binding proteins inhibit the growth of certain bacteria by reducing the
amount of available iron.
 Examples include
 Transferrin (found in blood and tissue fluids),
 Lactoferrin (found in milk, saliva, and mucus),
 Ferritin (found in the liver, spleen, and red bone marrow)
 Hemoglobin (found in red blood cells).
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44. 4. ANTIMICROBIAL PROTEINS (AMPS)
 Antimicrobial proteins (AMPs) are short peptides that have a broad
spectrum of antimicrobial activity.
 Examples of AMPs are
 Dermicidin (produced by sweat glands),
 Defensins and cathelicidins (produced by neutrophils, macrophages
and epithelial cells
 Thrombocidin (produced by platelets).
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45. NATURAL KILLER CELLS
 About 5–10% of lymphocytes in the blood are natural killer (NK) cells
 The NK cells bind to a target cell and cause the release of granules containing toxic
substances from NK cells
 Some granules contain a protein called perforin that inserts into the plasma membrane
of the target cell and creates channels (perforations) in the membrane.
 As a result, extracellular fluid flows into the target cell and,the cell bursts, a process
called cytolysis
 Other granules of NK cells release granzymes, which are protein-digesting enzymes
that induce the target cell to undergo apoptosis, or self-destruction
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47. PHAGOCYTES
 Phagocytes are specialized cells that perform phagocytosis, the ingestion of microbes
or other particles such as cellular debris
 The two major types of phagocytes are neutrophils and macrophages
 When an infection occurs, neutrophils and monocytes migrate to the infected area.
 During this migration, the monocytes enlarge and develop into actively phagocytic
macrophages called wandering macrophages.
 Fixed macrophages
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49. FEVER
 Fever is an abnormally high body temperature that occurs because the hypothalamic
thermostat is reset.
 It commonly occurs during infection and inflammation.
 Bacterial toxins elevate body temperature, by triggering release of fever-causing
cytokines
 Elevated body temperature
 Intensifies the effects of interferons,
 Inhibits the growth of some microbes,
 Speeds up body reactions that aid repair. Jegan

50. ADAPTIVE/ AQUIRED IMMUNITY
 The ability of the body to defend itself against specific invading agents such as bacteria,
toxins, viruses, and foreign tissues is called adaptive (specific) immunity.
 Two properties distinguish adaptive immunity from innate immunity:
 Specificity for particular foreign molecules (antigens)
 Memory for most previously encountered antigens so that a second encounter
prompts an even more rapid and vigorous response
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51.  White blood cells called lymphocytes originate in the bone marrow but migrate to
parts of the lymphatic system such as the lymph nodes, spleen, and thymus for
further development
 There are two main types of lymphatic cells, T cells and B cells.
 Adaptive immunity involves lymphocytes called B cells and T cells.
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52.  On the surface of each lymphatic cell are receptors that enable them to recognize
foreign substances. These receptors are very specialized - each can match only one
specific antigen
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53. TYPES OF ADAPTIVE IMMUNITY
 There are two types of adaptive immunity:
Cell-mediated immunity
Humoral immunity (Antibody-mediated immunity)
 Both types of adaptive immunity are triggered by antigens.
 In cell-mediated immunity, cytotoxic T cells directly attack invading antigens.
 In antibody-mediated immunity, B cells transform into plasma cells, which synthesize
and secrete specific proteins called antibodies (Abs) or immunoglobulins (Igs)
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54.  In most cases, when a particular antigen initially enters the body, there is only a small
group of lymphocytes with the correct antigen receptors to respond to that antigen
 Depending on its location, a given antigen can provoke both types of adaptive immune
responses.
 Some copies of the antigen may be present inside body cells (which provokes a cell-
mediated immune response)
 While other copies of the antigen may be present in extracellular fluid (which provokes
an antibody-mediated immune response).
 Thus, cell-mediated and antibody-mediated immune responses often work together to
get rid of the large number of copies of a particular antigen from the body.
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55. CELL-MEDIATED IMMUNITY
 Cell-mediated immunity is an immune response that does not involve antibodies, but
rather involves the activation of phagocytes, helper T cells, antigen-specific cytotoxic T-
lymphocytes, and the release of various cytokines in response to an antigen.
 Cell-mediated immunity is particularly effective against
 Intracellular pathogens, which include any viruses, bacteria, or fungi that are
inside cells
 Some cancer cells
 Foreign tissue transplants
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56.  Cell mediated immunity involves T-cells
 They are named T cells after the thymus, an organ situated under the breastbone.
 T cells are produced in the bone marrow and later move to the thymus where they
mature.
 There are two major types of mature T cells
 Helper T cells are also known as CD4 T cells, which means that, their plasma
membranes include a protein called CD4.
 Cytotoxic T cells are also referred to as CD8 T cells because their plasma
membranes contain a protein known as CD8.
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57.  When antigen invades a body they are present in huge number throughout the body
 But to this specific antigen there is less number of T-cells and B-cells
 Therefore, once each of these lymphocytes undergoes clonal selection.
 Clonal selection is the process by which a lymphocyte proliferates (divides) and
differentiates (forms more highly specialized cells) in response to a specific antigen.
 The result of clonal selection is the formation of a population of identical cells, called a
clone, that can recognize the same specific antigen as the original lymphocyte
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59. HELPER T-CELLS
 Helper T cells are the major driving force and the main regulators of the immune
defense.
 Their primary task is to activate B cells and killer T cells.
 However, the helper T cells themselves must be activated.
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60.  This happens when a macrophage or dendritic cell, which has eaten an invader, travels
to the nearest lymph node to present information about the captured pathogen.
 The phagocyte displays an antigen fragment from the invader on its own surface, a
process called antigen presentation.
 When the receptor of a helper T cell recognizes the antigen, the T cell is activated.
 Once activated, helper T cells start to divide and to produce proteins that activate B and
T cells as well as other immune cells.
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62. CYTOTOXIC T CELL (KILLER T CELL)
 The Cytotoxic T cell (killer T cell) is specialized in attacking cells of the body infected by
viruses and sometimes also by bacteria.
 It can also attack cancer cells.
 The killer T cell has receptors that are used to search each cell that it meets.
 If a cell is infected, it is swiftly killed.
 Infected cells are recognized because tiny traces of the intruder, antigen, can be found
on their surface
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64. HUMORAL IMMUNITY (ANTIBODY-MEDIATED IMMUNITY)
 Humoral immunity is the aspect of immunity that is mediated by macromolecules
found in extracellular fluids such as secreted antibodies, complement proteins, and
certain antimicrobial peptides.
 Humoral immunity is so named because it involves substances found in the humors, or
body fluids
 In Humoral immunity (antibody-mediated immunity), B cells transform into plasma
cells, which synthesize and secrete specific proteins called antibodies (Abs) or
immunoglobulins (Igs)
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65.  The B lymphocyte cell searches for antigen matching its receptors.
 If it finds such antigen it connects to it, and inside the B cell a triggering
signal is set off.
 The B cell now needs proteins produced by helper T cells to become fully
activated.
 When this happens, the B cell starts to divide to produce clones of itself.
 During this process, two new cell types are created, plasma cells and B
memory cells
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66. PLASMA B-CELL
 The plasma cell is specialized in producing a specific protein, called an antibody, that will
respond to the same antigen that matched the B cell receptor.
 Antibodies are released from the plasma cell so that they can destroy invader cells.
 Plasma cells produce antibodies at an amazing rate and can release thousands of antibodies
per second.
 When the Y-shaped antibody finds a matching antigen, it attaches to it.
 The attached antibodies serve as an appetizing coating for eater cells such as the macrophage.
 Antibodies also neutralize toxins and incapacitate viruses, preventing them from infecting new
cells.
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67. MEMORY B-CELLS
 The Memory Cells are the second cell type produced by the division of B cells.
 These cells have a prolonged life span and can thereby "remember" specific intruders.
 T cells can also produce memory cells with an even longer life span than B memory cells.
 The second time an intruder tries to invade the body, B and T memory cells help the
immune system to activate much faster.
 The invaders are wiped out before the infected human feels any symptoms.
 The body has achieved immunity against the invader.
Jegan

69. THANK YOU