Immunology 1 - intro to immunology Flashcards

1
Q

4 differences between the inate and adaptive immune response

A

innate - rpaid, already from birth, not as specific, no memory - same response with re exposure, ddetects alterations in haemostasis

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2
Q

which innate immune cells get altered in the presence of bacteria?

A

Neutrophils and macrophages. Natural killer cells, dendritic cells, mast cells

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3
Q

innate immune cells

A

neutrophils, basophils, eosinophil, monocyte (macrophage, denritic cells)

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4
Q

which are in the blood?

A

baso, neutro, eosino, monocyte

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5
Q

which are in the tissues

A

macrophage, dendritic cells, mast cells

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6
Q

how are antigens detected?

A

cell sufrace receptors

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7
Q

Which substances are released from these cells once they recognise the invasion?

A

cytokines

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8
Q

what effect do cytokines have in helping the immune response?

A

vasodulation, increased vascular permiability, recruiting other immune cells

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9
Q

By which ‘killing mechanism’ do these cells try to eradicate an invader?

A

phagocytosis

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10
Q

other funcitons of the innate immune system

A

antigen presentation, inflammation, recruit cells, opsonisation, lysis

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11
Q

define a antigen and antibody?

A

ag - A molecule capable of inducing an immune response

ab - A glycoprotein produced by B lymphocytes that binds antigens with a high degree of specificity and affinity

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12
Q

what does MH1 and MH2 bind?

A

1 to 8, 2 to 4 (CD4/CD8)

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13
Q

what happens once t cells differentiate?

A

T cells differentiate into naïve T cells within the thymus. These naïve T cells (either CD4+ or CD8+) then move to the lymph nodes where they encounter antigen presented by dendritic cells. At that point, if they recognise an antigen, they will proliferate into T helper cells (if CD4+) or cytotoxic T cells (if CD8+)

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14
Q

how to dendritic cells work?

A

Present antigen via MHC2, Sentinel for the immune system. Excellent at activating adaptive immune system. Internalizes pathogen and processes it into peptides which it presents (antigen). T cells which have not seen antigen before (naïve) are activated

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15
Q

name the adaptive immune cells

A

small lymphocyte –> T or B –> B matures to plasma cells

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16
Q

where do t cells mature?

A

bone marrow and then thymus

17
Q

where do b cells mature?

A

bone marrow and then thymus. B and T cells then migrate to secondary lymphoid organs, where they encounter antigen

18
Q

what do CD4+ T cells differentiate into?

A

differentiate into distinct subsets of effector cells in response to antigen, co-stimulators, and cytokines. TH1, TH2, TH17

19
Q

function of THELPER1 cells

A

secretes IFNgamma, macrophage activation, igG production, host defence - intracellular microbes, role - autoimmune diseases, tissue damage, chronic infecrtions

20
Q

what are cytokines?

A

Large and heterogeneous soluble proteins
Communication system – act locally or at a distance
Regulate and co-ordinate the cells of innate and adaptive immunity ie regulate immune responses
Produced during normal haematopoiesis
Produced in response to microbes, tissue damage or other antigens
Produced by many cell types – esp macrophages and T helper cells

21
Q

what else can TH cells do in regard to B cells?

A

Some Th cells will help the B cell response so that B cells produce the correct antibody isotype and the antibody affinity improves

22
Q

how do CD8+ (cytotoxic) cells kill?

A

By inducing apoptosis in a targeted cell

23
Q

NK cells…

A

NK cells (innate system) are important against intracellular pathogens
NK cells may respond via their activating receptors to activating ligands on infected cells in TB or to antibody-tagged cells or directly to bacteria via TLR2
They can kill infected cells
They produce IFN-g which will help to stimulate macrophages, TH1 cells and CD8+ cytotoxic T cells
They are especially important if T cell response is not optimal

24
Q

outline the different immunoglobulin isotypes?

A

igM - best activating complement, igG - can cross the placenta, igA (dimer) - contained in secretions, igE - parasitic infections and allergy, igD

25
Q

how do B cells modulate immune responses?

A

Production of M. tuberculosis-specific antibodies can mediate the formation of immune complex that can modulate the functions of effector cells such as dendritic cells and macrophages. It remains to be demonstrated whether specific neutralizing antibodies exist. B cells can serve as antigen presenting cells to influence T cell activation, polarization, and effector functions and the establishment of T cell memory. B cells can also modulate the functions of granulomatous immune cells. In concert, these antibody-dependent and independent functions of B cells play an important role in determining disease outcome in terms of the elimination of control of bacteria, as well as the development of immunopathology that could damage tissues and promote dissemination

26
Q

what are the effector functions of antibodies?

A

Antibodies are produced by the activation of B lymphocytes by antigens and other signals (not shown). Antibodies of different heavy chain classes (isotypes) perform different effector functions.
Complement is an enzyme cascade system which can be activated to help the immune response - leading to inflammation.,
Opsonization is the tagging of a microbe so that it is phagocytosed more easily and efficiently. Antibodies and complement fragments can be opsonins.
Neutralization on microbes and toxins
Lysis of microbes
phagocytosis of microbes opsonized with complement fragments.

27
Q

OUTLINE ANTIBODY MEDIATED IMMUNITY

A

When a foreign antigen is first encountered, a lag phase occurs while activated B cells are differentiating into plasma cells. During the lag phase, no antibodies are produced. Once plasma cells have formed, a low volume of IgM antibodies are released to neutralise this initial infection, although small amounts of IgG can also be produced. Memory B cells that recognise the specific antigen are also produced.

If the same antigen is encountered again, there is an accelerated response initiated by these memory B cells which immediately recognise this antigen. Once activated, memory B cells quickly proliferate and create plasma cells, causing the fast release of a high volume of IgG antibodies specific to this antigen, as well as a low amount of IgM.
After the primary infection by a pathogen, a small pool of long-lived memory B and T cells specific to the pathogen’s antigen remain quiescent within the body. Memory cells can lie dormant for many years but are poised to respond rapidly if reinfection occurs. This is referred to as immunological memory.

Memory B cells are vital for generating an accelerated and more potent antibody-mediated immune response in secondary immune responses.

Memory T cells can either express CD4 or CD8, and respond rapidly if the host is re-exposed to a previously encountered antigen.