Immunity Flashcards

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1
Q

Define immunity

A

Immunity is the ability of an organism to resist disease by identifying and destroying pathogens.

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2
Q

Explain the types f immunity

A

Innate Immunity (Non-specific): Provides immediate defense against infection and is not specific to particular pathogens.

Adaptive Immunity (Specific): Develops more slowly and provides specific responses to pathogens, including memory for future responses.

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3
Q

Explain the physical barrier in innate immunity

A

Skin and mucous membranes act as a first line of defense by physically blocking pathogens from entering the body.

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4
Q

Explain the chemical barrier in innate immunity

A

Lysozymes: Enzymes found in tears, saliva, and mucus that can break down bacterial cell walls.

Stomach Acid: Hydrochloric acid in the stomach kills many ingested pathogens.

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5
Q

Explain the 4 cellular defense in innate immunity

A

Phagocytes: Cells that engulf and digest pathogens.
Neutrophils: The most abundant white blood cells that rapidly respond to infection.
Macrophages: Large phagocytic cells that engulf and digest pathogens and dead cells.
Natural Killer (NK) Cells: Destroy infected or cancerous cells by inducing apoptosis.(programed call death)

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6
Q

Explain the process of inflammatory response

A

Injury/Pathogen Entry: Pathogens enter through a cut or injury.
Release of Chemical Signals: Damaged cells release histamines and other chemicals.
Increased Blood Flow: Blood vessels dilate, causing redness and heat.
Increased Permeability: Blood vessels become more permeable, allowing immune cells and fluids to enter the tissue, causing swelling.
Phagocyte Recruitment: Phagocytes move to the site of infection to engulf pathogens.
Fever: Elevated body temperature helps inhibit pathogen growth and enhances immune cell function.

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7
Q

What are the antimicrobial protein involved in innate immunity

A

Interferons: Proteins released by virus-infected cells to help protect neighboring cells from viral infection.
Complement System: A group of proteins that enhance immune responses by promoting phagocytosis, inflammation, and cell lysis.

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8
Q

what is under adaptive immunity?

A

self and non-self recognition

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9
Q

What are the 2 main components involved in the adaptive immunity?

A

Lymphocytes: White blood cells involved in adaptive immunity, including B cells and T cells.
Antigens: Molecules that trigger an immune response.

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10
Q

What are the components involved in humoral immune response?

A

B Cells: Lymphocytes that produce antibodies.
Plasma Cells: Differentiated B cells that secrete large quantities of antibodies.
Memory B Cells: Long-lived cells that quickly respond to future exposures to the same antigen.

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11
Q

Explain the process of humoral immune response?

A

i. Antigen presenting cell @ APC (dendritic cell / macrophage / B cell)
phagocytizes pathogen and degrades it.

ii. Fragment of foreign antigen binds to the class II MHC protein forming MHC-antigen complex and displayed on the surface of APC

iii. TH cell with its antigen receptor and accessory protein, CD4 binds to the complex of APC

iv. APC releases interleukin 1 (IL-
to activate T_{H} cell

v. Activated T_{H} cell releases IL-2

vi. T_{H} cell proliferates producing activated T_{H} cells and memory T_{H} cells

vii. Once antigens are bound to B cell receptor (antibody) in the B cell membrane, the B cell displays those antigens that bound to the class 11 MHC molecule on the surface of it’s plasma membrane

viii. Activated T_{H} bind to the sensitized B cell

ix. Activated T_{H} cell will release IL-2 that co-stimulate the sensitized B cell and trigger its activation..

x. The activated B cell then proliferates or divides mitotically, producing memory B cells and plasma cells (effector cells).

xi. Plasma cells secretes antibodies.

xii. Antibody-antigen interaction occurs.

xiii. Triggers processes leading to pathogen destruction

xiv. Memory B cells are long-lived cells that can give rise to effector cells if the same antigen is encountered later in life

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12
Q

What are the components involved in cell mediated immunity

A

T Cells: Lymphocytes involved in directly attacking infected cells.
Helper T Cells (Th): Activate B cells and cytotoxic T cells.
Cytotoxic T Cells (Tc): Destroy infected cells by inducing apoptosis.
Regulatory T Cells (Treg): Help modulate immune responses and prevent autoimmunity.
Memory T Cells: Long-lived cells that respond to future exposures to the same antigen.

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13
Q

how specific immunity is aquired by cell mediated response

A

Infected cells, cancerous cells or leucocytes which have phagocytosed foreign material become antigen presenting cells (APC)

APC displays fragments of antigens on their cell surface membranes via MHC( MHC stands for Major Histocompatibility Complex. It’s a set of molecules found on the surfaces of cells that are essential for the immune system to recognize foreign substancesmolecules in their membranes).

When a helper T-cell (T_{H}) encounters and recognises the MHC-antigen complex T_{H} is stimulated to divide rapidly and produce activated TH cells and memory cells.

T_{H} cells have CD4 proteins on their membranes which bind with the MHC molecule on the APC.

interlukein 1 secreted by apc activates helper cell to secrete il2.

Activated T_{H} cells secrete cytokines that promote the activation of cytotoxic T-cells

(T_{C}) Tc cells have CD8 surface proteins that bind to the target cells, which are infected body cells or cancerous cells.

Activated T_{C} cells release perforin and proteolytic enzymes.

Perforin makes pores in the target cell membranes
while the proteolytic enzymes cause the death of the target cell.

After destroying the target cells, the T_{c} cells can go on to attack other infected cells.

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14
Q

explain the function of plasma cells and memory cells

A

Plasma cells secrete antibodies specific for the antigen that stimulated the activation of the B-lymphocytes.

Each plasma cell produces and secretes about 2000 antibody molecules per second.

The life span of the plasma cell is 4-5 days.

Memory cells are long-lived and are capable of rapid proliferation and differentiation when they encounter the same antigen in subsequent infections.

Memory cells responsible for rapid and pronounced secondary response which is the reason why individual rarely develop the symptoms of a disease more than
once.

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15
Q

Explain antigen

A

-Antigens are the molecules usually proteins, polysaccharides or glycoproteins

-carried on the surface of cells that cause antibody formation.

-All cells have antigen markers in their cell surface membranes

  • but the body can distinguish between its own antigens (self) from foreign antigens (non-self).
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16
Q

Explain about antibidy

A

-Antibody is a specific protein (immunoglobulin)

  • that recognises and binds to specific antigens

Antibodies either neutralise the antigen or tag cells that are antigenic.

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17
Q

Explain about epitope

A

These antigenic determinants are specific sequences of amino acids that confer a specific shape to the antigen molecule,which is then recognised by an antibody or T-cell receptor. An antigen may have several different epitopes on its surface.As a result, different antibodies may bind to a single antigen.

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18
Q

Explain about major histocompatibility complex

A

A set of closely-linked genes which code for a set of proteins (antigen markers) found on the surface of cells.

MHC Class I antigens are carried by most nucleated cells and are Important in self /non-self recognition.

MHC Class II antigens are mostly found on B-cells, macrophages and some T-cells.

MHC Class III proteins are components of the complement system.

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19
Q

what is the diffrence between specific and non specific

A

Non-specific defence,
- mechanisms do not target particular pathogens
-They are defence that either stop pathogens from entering the body or a general response to the presence of a foreign (pathogen) in the body

-Specific
- involve the production of antibodies against particular pathogens

20
Q

when do non specific antibodies operate and specific antibosies operate

A

Non-specific defence mechanisms can be divided into first-line and second- line defences

P2 First-line defences are barriers such as skin and mucous membranes as well as the action of cilla and chemical secretions from the stomach, vagina and

urinary tract. P3 To prevent pathogens. from entering the body

P4 Second-line defences include inflammation and phagocytosis. P5 These methods operate once pathogens have managed to enter the body

P6 Specific defence mechanisms operate after entry of pathogens.

P7 They target specific pathogens, produce specific antibodies to destroy them.

21
Q

Explain about cytokines

A

Peptides and proteins that regulate many cell activities (growth and repair)and act as signals in both the specific and non-specific immune responses.

Examples of cytokines include interferons and interleukins

22
Q

Explain the concept of self and non self

A

Self

P1 The lymphocytes in the body which have the ability to detect any foreign substance/protein that is incompatible with it

P2 If foreign substance is compatible to body cells/has class 1 MHC protein or antigen found on the surface of most nucleated cells, no immunity response Is triggered

P3 The foreign substance is self substance and is not rejected

Non-self

P4 If the class | MHC protein is detected as an antigen.

P5 The foreign substance is considered as a non-self substance

P6 trigger an immune response by producing antibodies that attack foreign tissue, eventually destroy it

22
Q

Explain the inflammatory response to help body overcome pathogen

A

P1 During inflammation blood circulation to the affected area is increased.

P2 Blood vessels dilate

P3 White blood cells leak out of the blood vessels into the surrounding tissue

P4 they engulf foreign materials, cells and toxins.

P5 Histamines and prostaglandins are produced by the damaged cells encourage the inflammatory response.

23
Q

Function of cytotoxic T cell

A

Attack virus infected cell and cancerous cell, destroys cell with foreign antigen

24
Q

Explain function of helper T cell

A

Stimulate immune response by b and cytotoxic cells

25
Q

Explain function of cytotoxic t cell

A

destroys cell with foreign antigens on the surface ,attack virus infected cell and cancerous cell

26
Q

explain function of suppresor cell

A

inhibits immune response by other lymphocyte

27
Q

diffreantiate role of t lymphocyte and b lymphocyte

A

-where it is involved
-where is made and where it is matured
-how it response

28
Q

compare cell mediated and humoral response

A
29
Q

state and explain five types of immunoglobin

A

Ig M-P1- First antibody secreted during primary immune response

P2- promotes agglutination, precipitation & activates complement reaction

IgA-defends against inhaled / ingested pathogens

P4- is secreted into respiratory, digestive, urinary, reproductive

IgD–Present on the surfaces of B cells and serves as antigen. receptor

P6- has a critical role in maturation of B cells and helps activate B

IgG-crosses the placenta and protects the fetus and later the

newborn baby

P8-secreted during secondary response,

P9- neutralizes antigens, promotes phagocytosis and activates

lgE-P10- binds to mast cells and trigger the release of histamine

P11-Histamine is released when antigen binds to Ig E on a mast cell.

P12-Histamine triggers allergy symptoms & inflammation

P13- responsible for an immune response to invading parasitic worms.

30
Q

explain the function of b cell

A

-proliferates to plasma cell and memory b cell
-plasma cell secrete antibodies
-activated by helper t cell

31
Q

describe the basic structure of antibody

A

the antibodies are Y-shaped molecules.

P2 composed of two identical long polypeptides (heavy chain).

P3 and two identical short polypeptides (light chains).

P4- held together by disulphide bridges.

P5- both light and heavy chains have a constant region and a variable regio

P6 the constant region is the same in all antibodies

32
Q

explain the development of b cell

A

P5 Some of the lymphocytes mature in the bone marrow, develop into B cell P6 The T cells and B cells reside/located in separate regions of the spleen/lymph nodes/other lymph tissues.

33
Q

explain the development of t cell

A

Stem cells in the bone marrow produce immature lymphocytes
during fetal stage.

P3 Some migrate to the thymus gland, stay there until mature then develop into Tcell.

T cell differentiate into cytotoxic T cell, helper T cell and suppressor T cell.

34
Q

explain 5 example of antigen antibody reaction

A

-opsonisation- these antibodies attach to the wall of the viruses and make them easily recognised and engulfed by phagocytes

-precipitation-cross linking of soluble antigen molecules

-agglutination-clumping of bacteria to enhance phagocytosis

-neutralisation- antibodies can neutralise toxin by binding to certain part of toxin

-complement fixation-the activation of series of protein complement leading to lysis of pathogen

-Lysis-the antibodies react with antigen to dissolve them

35
Q

what are the similarities

A

-both produce memory cell
-both involve in secondary and primary response
-both able to attach to target cells

36
Q

what are 4 types of transplant

A

-allograft
-autograft
-isograft
-xenograft

37
Q

Explain the mechanism of HIV that cause immune suppression

A

HIV binds to the host cell/helper T cell
membrane.

P2 Viral RNA and reverse transcriptase are release into helper T cell (by endocytosis).

P3-reverse transcriptase is use to synthesise a single-stranded DNA using viral RNA as template (a patern)

The single-stranded DNA is used for the synthesis of a double-stranded viral DNA/

Viral DNA is inserted into the host [1]
DNA/chromosomes. host cell divides.

P6- The viral DNA provirus may remain dormant

P7- The host cell then synthesise new viral protein and viral RNA (which are assembled into HIV).

P8. The new HIV then released from the host cell

P9. The host cell dies // destruction of other helper T cells.

P10 - suppress the dies // destruction of cause many secondary infectionn

38
Q

Explain the first and second phase of in the aids progress

A

First phase-most individuals have no symptoms. although some may have flu-like symptoms, skin rash and swollen lymph nodes.

Second phase- Production of anti-HIV rises in the bloodstream. Although the level of HIV in the blood falls. HIV replication continues in the lymph nodes. This phase may last from a few weeks to 13 or more years.

39
Q

Explain the third and fourth phase

A

Third phase- AIDS-related complex refers to the many opportunistic infections which affect the patient. These include common bacterial, fungal and viral infections such as oral and genital herpes and athlete’s foot. The patient may lose weight and there is a significant drop in the number of TH cells.

Fourth phase- More opportunistic infections and the development of secondary cancers. Kaposi’s sarcoma and non-Hodgkin’s lymphoma are common. The virus infects the nervous system causing AIDS dementia complex. By this time, there is almost total loss of cellular activity.

40
Q

explain why healthy kidney is rejected

A

-foregin tissue contain non-self antigens codded by MHC genes
-first way
-cytotoxic t cell which have antigen receptor attack the transplant tissue by relesing perforin
-perforin makes pores in target cell
-second way
-transplanted tissue thaat have lysed attracts circulating antibodies
-antibodies act on foreign tissue in diffeant way like neutralistion,agglutination..etc

41
Q

explain steps to overcome rejection

A

-tissue from patient and potential donors are typed and matched closely as possible
-use immunosuppresent drugs like FK506
-x rays radiation of bone marrow and lymph tissue to inhibit production of white blood cell.

42
Q

explain the autoimmune disoder

A

-immune system unable to diffreantiate self and non self protein
-the body produces antibodies against its own cell
-immune system destroys normal healthy tissue
-may effect skin brain joints and other organs

43
Q

explain the cause of sle

A

(a) Normally, our immune cells ignore our own body tissues to avoid attacking them. However, when our body is fighting off invaders like viruses, bacteria, or allergens, sometimes these immune cells can get mistakenly activated and start reacting to our own tissues.

(b) This mistaken reaction can be made worse by factors like exposure to ultraviolet (UV) light or certain medications.

Part 5:
(a) When these immune cells start attacking our own cells, it leads to the destruction of those cells. This destruction releases cell contents like DNA and proteins, particularly from the cell nucleus.

(b) The immune system then makes antibodies (proteins that usually fight off infections) that target these released nuclear proteins.

(c) These antibodies clump to become antibody-protein complexes which stick to surfaces and damage blood vessels in critical areas of the body, such as the glomeruli of the kidney; these antibody attacks are the cause of SLE

44
Q
A