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immunology > course 3_slides > Flashcards

course 3_slides Flashcards

1
Q

Describe the role of CD8+ T lymphocytes in immune reactions against tumors.

A

CD8+ T lymphocytes kill tumor cells by recognizing tumor antigens presented via MHCI. They do not require the presence of costimulatory molecules to trigger killing once activated

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2
Q

What is the function of NK cells in immune reactions against tumors?

A

NK cells kill tumor cells lacking MHCI, kill tumor cells covered with antibodies via ADCC, and release cytokines that stimulate T cells and promote maturation of APCs.

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3
Q

Define LAK cells and their role in immune reactions against tumors.

A

LAK cells, or lymphokine activated killer cells, are IL-2-activated NK cells derived from tumor infiltrating lymphocytes. They are involved in immunosurveillance and killing of tumor cells. In vitro

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4
Q

How do CD4+ T cells contribute to immune reactions against tumors?

A

CD4+ T cells produce helper cytokines for efficient formation of CD8+ T cells, aiding in the immune response against tumors.

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5
Q

Describe the evidence for the involvement of NK cells in immunosurveillance.

A

Real-life evidence includes the higher incidence of EBV-associated lymphoma in patients lacking NK cells, as well as the relative lower incidence of spontaneous tumors in immune deficient patients lacking T cells.

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6
Q

Describe the process of CD8+ CTL-mediated immune reaction against tumors.

A

CD8+ CTLs mediate immune reaction against tumors through cross-priming by APC, which is necessary due to the lack of costimulatory molecule expression on the tumor cell. APC activates CTL via MHCI/peptide complex and costimulation.

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7
Q

What is the role of CD4+ helper cells in the immune reaction against tumors?

A

CD4+ helper cells are activated by APC via MHCII/peptide complex, leading to cytokine production. They help in CTL differentiation, activation, and proliferation.

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8
Q

How is cross-priming by APC important in the CD8+ CTL-mediated immune reaction against tumors?

A

Cross-priming by APC is necessary due to the lack of costimulatory molecule expression on the tumor cell, and it is essential for activating CTLs via MHCI/peptide complex and costimulation.

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9
Q

Describe the process of target cell-killing by CD8+ CTL.

A

CD8+ CTLs target and kill specific cells, such as infected or cancerous cells, through a process of intratumoral killing that occurs at a slow rate of approximately 1 killing event every 6 hours per CTL.It involves FasL/Fas complex CD95

apoptotic signalling though Fas receptors - tumor necrosis receptor family

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10
Q

What is the difference in the surveying of the tumor by CTL and NK cells?

A

CTL and NK cells survey different regions of the tumor, indicating that they have distinct roles in immune surveillance within the tumor environment.

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11
Q

Describe the role of NKT cells in immune reactions against tumors.

A

NKT cells are important for immunosurveillance and can kill tumor cells directly through Fas/FasL dependent mechanisms. They also contribute to anti-tumoral effects by activating NK cells and inhibiting angiogenesis via inhibition of TAM.

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12
Q

How do NKT cells contribute to anti-tumoral effects?

A

NKT cells contribute to anti-tumoral effects by directly killing tumor cells, indirectly killing via activation of NK cells, and inhibiting angiogenesis through inhibition of TAM (confirmation needed).

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13
Q

Describe the antitumor activities of invariant NKT (iNKT) cells.

A

iNKT cells, also known as Type I NKT cells, express a semi-invariant TCR that recognizes lipid antigens presented on CD1d. These cells have been shown to exhibit antitumor activities.

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14
Q

Describe the role of M1 macrophages immune reactions against tumors.

A

M1 macrophages are activated by IFN-g and kill tumor cells using mechanisms similar to those used to kill micro-organisms, such as releasing lysosomal enzymes, reactive oxygen and nitrogen species. They also produce TNF-a, which can lead to tumor regression by eliciting intratumoral thrombosis and enhancing MHCI expression on tumor cells.

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15
Q

What are the effects of TNF-a and IFN-g on tumor cells in the context of immune reactions against tumors?

A

TNF-a and IFN-g enhance the expression of MHCI on tumor cells. IFN-g also activates macrophages to kill tumor cells.

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16
Q

How does IL-12 support immune responses against tumors?

A

IL-12 supports strong T H 1 and CTL responses, and its deficiency results in more papillomas in animals. Administration of IL-12 protects mice from chemically induced tumors.

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17
Q

Describe the role of antibodies in immune reactions against tumors.

A

Antibodies activate the complement system, mediate ADCC and ADCP, and may block CTL access to tumor antigens.

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18
Q

What is the significance of B cells in the immune response against tumors?

A

B cells are essential for the formation of tertiary lymphoid structures (TLS) that promote local anti-tumoral immune responses, and intra-tumoral B cells correlate with good prognosis.

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19
Q

How do tertiary lymphoid structures (TLS) contribute to the immune response against tumors?

A

TLS are typical features of chronic inflammation, require recruitment of Tfh cells for establishment, and correlate with good prognosis in cancer patients.

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20
Q

Define Tfh cells and their role in the immune response against tumors.

A

Tfh cells, or T follicular helper cells, are required for the establishment of tertiary lymphoid structures (TLS) that promote local anti-tumoral immune responses.

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21
Q

Do antibodies play a significant role in the immune response against tumors?

A

Yes, antibodies activate the complement system, mediate ADCC and ADCP, and may block CTL access to tumor antigens.

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22
Q

Describe tumor infiltrating B cells (TIB cells).

A

Tumor infiltrating B (TIB cells) refer to B cells have infiltrated the tumor microenvironment. They play a role in the tumor immune response and can have both pro-tumor and anti-tumor effects.

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23
Q

How do tumor infiltrating B cells (TIB cells) impact the tumor immune response?

A

Tumor infiltrating B cells (TIB cells) can have both pro-tumor and anti-tumor effects. They can contribute to the tumor immune response by influencing the tumor microenvironment and interacting with other immune cells.

antibodyproduction,
support Th1 cells and CTL,
CD4 and CD8 activation
tumor cell lysis through killer b cell granzyme B
survival of CTL
suppression of effector cell and promotion of t regs
TLS formation - CXCL13

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24
Q

Describe the role of Tfh in TLS formation in the context of breast cancer prognosis.

A

Tfh produce the chemokine CXCL13, which is required for TLS formation and stimulates anti-tumoral Th1 cell differentiation, promoting anti-tumoral immunity.

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25
Q

Define the correlation between low signal for Tfh, CXCL13, and Th1 with breast cancer survival, especially in the HER2+ group.

A

Low signal for Tfh, CXCL13, and Th1 correlates with low survival, particularly in the HER2+ group.

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26
Q

How do TLS contribute to breast cancer prognosis?

A

TLS promote anti-tumoral immunity and stimulate anti-tumoral Th1 cell differentiation, impacting breast cancer prognosis.

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27
Q

Describe how some tumor cells evade immune recognition and activation.

A

Some tumor cells evade immune recognition and activation by reducing MHC expression, having mutations in genes for MHC class I expression, and decreasing expression of NK activating receptor ligands.

28
Q

Define the role of TAP, β2-microglobulin, and IFN-γ mutations in tumor cells.

A

Mutations in TAP, β2-microglobulin, and IFN-γ can lead to insensitivity in tumor cells, making them poor targets for immune cells like CTLs and NK cells.

29
Q

How do decreased expression of NK activating receptor ligands affect tumor cells?

A

Decreased expression of NK activating receptor ligands makes tumor cells poor targets for NK cells, reducing their susceptibility to immune attack.

30
Q

Define clonal anergy in T cells.

A

Clonal anergy in T cells refers to a state of immune tolerance where T cells become unresponsive to antigens due to lack of proper costimulatory signals.

31
Q

How do some tumors evade immune recognition and activation?

A

Some tumors evade immune recognition and activation by providing poor costimulatory signals in the tumor stroma, such as mutations or downregulation of second signal molecules like B7.1/CD80 or B7.2/CD86 on APCs and CD28 on T cells.

32
Q

What do recently approved therapies aim to do in the context of the immune response to cancer?

A

Recently approved therapies aim to enhance costimulation to anti-tumor T cells in order to improve the immune response to cancer and target cancer cells more effectively.

33
Q

How do tumor cells upregulate anti-apoptotic mediators to evade immune killing in the context of the immune response to cancer?

A

Tumor cells upregulate anti-apoptotic mediators as a mechanism to evade immune killing by resisting programmed cell death, thereby promoting their survival and proliferation.

34
Q

Describe the three phases proposed in the immune response to cancer.

A

The three phases proposed are elimination, equilibrium, and escape.

35
Q

Define immunoediting in the context of cancer.

A

Immunoediting refers to the selection pressure of the immune system on tumor cells, where those that acquire characteristics allowing escape from the immune system have a survival benefit.

36
Q

How does the immune response to cancer both protect against and promote tumor growth?

A

The immune response can eliminate mutated cells in the elimination phase, but those that escape immune recognition in the equilibrium and escape phases can thrive and spread, promoting tumor growth.

37
Q

What happens during the equilibrium phase of the immune response to cancer?

A

During the equilibrium phase, elimination of mutated cells is not complete, and some tumor cells arise. Those that acquire characteristics allowing escape from the immune system have a survival benefit.

38
Q

Do all tumor cells accumulate enough mutations to be invisible to the immune system?

A

No, only some tumor cells accumulate enough mutations to be invisible to the immune system and induce neovascularisation, allowing unrestrained growth.

39
Q

Describe the components of an anti-tumoral microenvironment.

A

Type I IFN, TNF-a, Th1 (IL-12, IFNg), M1 macrophages, NK cells, CTL, N1 neutrophils, tertiary lymphoid structures, HEV.

40
Q

What are the components of a pro-tumoral microenvironment?

A

IL-10, TGFbeta, IDO, M2 macrophages, MDSCs, T reg, chronic inflammation.

41
Q

Define the key components of cancer-related inflammation.

A

Cancer-related inflammation includes the infiltration of leukocytes, presence of soluble mediators (cytokines and growth factors), tissue remodeling, and angiogenesis.

42
Q

How does chronic inflammation predispose individuals to different forms of cancer?

A

Epidemiological studies indicate that chronic inflammation predisposes individuals to different forms of cancer, such as colon cancer (inflammatory bowel diseases), stomach cancer (Helicobacter pylori infection), and liver cancer (viral hepatitis).

43
Q

Describe the role of cancer-related inflammation in promoting tumor growth and progression.

A

Cancer-related inflammation promotes tumor growth and progression by contributing to the tumor microenvironment through features such as leukocyte infiltration, presence of soluble mediators, tissue remodeling, and angiogenesis.

44
Q

Describe the relationship between chronic inflammation and cancer.

A

Chronic inflammatory responses can promote cancer by increasing cellular stress signals, leading to genotoxic stress, inducing proliferation, and stimulating the formation of new blood vessels.

45
Q

Define how chronic inflammation can lead to genotoxic stress.

A

Chronic inflammation can lead to genotoxic stress by increasing mutation rates in cells.

46
Q

How does inflammation contribute to greater tumor-cell invasion into surrounding tissues?

A

Inflammation is pro-angiogenic, stimulating the formation of new blood vessels, which allows for greater tumor-cell invasion into surrounding tissues.

47
Q

Do growth factors/cytokines released by cells in chronic inflammation induce proliferation?

A

Yes, growth factors/cytokines released by cells in chronic inflammation often induce proliferation.

48
Q

Describe the role of macrophages in solid tumors.

A

Macrophages constitute the major inflammatory infiltrates of most solid tumors.

49
Q

What effect does overexpression of CCL2 in murine fibrosarcoma have on tumor growth?

A

It leads to more macrophages and increased tumor growth.

50
Q

How does deletion of CSF-1 in mammary carcinoma affect tumor progression?

A

It leads to TAM depletion, delayed tumor angiogenesis, delayed progression, and reduced pulmonary metastasis.

51
Q

Define the impact of systemic depletion of macrophages by clodronate liposomes on tumor growth.

A

It results in reduction in tumor growth and angiogenesis, and a lower number of cancer stem cells.

52
Q

What factors induce M1 to M2 transition in tumors, produced by tumor cells and tumor infiltrating T(reg) cells and TAMs?

A

TGFbeta, IL-10, M-CSF.

53
Q

Define M1 and M2 macrophages.

A

M1 macrophages are pro-inflammatory and involved in host defense, while M2 macrophages are anti-inflammatory and contribute to tissue repair and remodeling.

54
Q

Describe the roles of RNI/ in the context of immune response and inflammation.

A

Reactive nitrogen/oxygen species play a crucial role in immune response and inflammation, contributing to the regulation of various physiological processes and defense mechanisms.

55
Q

Define TAMs and their significance in cancer onset and progression.

A

TAMs, or tumor-associated macrophages, are a type of immune cells that play a significant role in the onset and progression of cancer by influencing the tumor microenvironment and promoting tumor growth and metastasis.

56
Q

How do MSCs and CSCs differ in their functions and characteristics?

A

Mesenchymal stem cells (MSCs) and cancer stem cells (CSCs) differ in their functions and characteristics, with MSCs being multipotent cells involved in tissue repair and regeneration, while CSCs are a subpopulation of cancer cells with self-renewal and tumor-initiating capabilities.

57
Q

Describe the role of TAMs in cancer onset.

A

TAMs contribute to cancer onset through cancer-related inflammation, release of reactive oxygen and nitrogen species causing DNA damage, and the release of cytokines that act as survival factors for transformed cells.

58
Q

What are the ways in which TAMs promote tumor progression?

A

TAMs promote tumor progression by promoting angiogenesis, invasion, metastasis, and tumor growth through the release of cytokines and growth factors.

59
Q

How do TAMs influence the response to therapy in cancer treatment?

A

TAMs influence the efficacy of response to chemotherapy and can alter the vasculature, leading to less efficient chemotherapy delivery.

60
Q

Define the immune regulatory role of TAMs in established tumors.

A

TAMs have an immune regulatory role in established tumors by promoting M2, Th2, and Treg cells while inhibiting Th1 and M1 cells.

61
Q

What is the significance of IL-23 and the Th17 pathway in cancer progression?

A

IL-23 and the Th17 pathway key role in many cancer

62
Q

What are the specific cytokines and growth factors released by TAMs to promote tumor progression?

A

TAMs release cytokines and growth factors such as VEGF, MMP-9, CXCL8, IL-4, IL-10, TGFb, and EGF to promote angiogenesis, invasion, metastasis, and tumor growth.

63
Q

How do TAMs influence the recruitment of stromal cells in the tumor microenvironment?

A

TAMs influence the recruitment of stromal cells, such as fibroblasts, through the release of cytokines and growth factors.

64
Q

Describe the impact of TAMs on chemotherapy-induced expression of CCL2 and CSF-1.

A

TAMs can induce the expression of CCL2 and CSF-1 in response to chemotherapy, leading to more TAM recruitment and potentially impacting the efficacy of chemotherapy.

65
Q

Describe the role of RNI/ROI in tumor progression.

A

Reactive nitrogen/oxygen species (RNI/ROI) are involved in tumor progression, contributing to the regulation of the tumor microenvironment and immune response.

66
Q

Define ECM and its significance in tumor progression.

A

ECM stands for extracellular matrix, which plays a crucial role in tumor progression by providing structural support, regulating cell behavior, and influencing the tumor microenvironment.

immunology (11 decks)

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