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Systems Physiology > Cancer and the Immune System > Flashcards

Cancer and the Immune System Flashcards

1
Q

What are the role of the immune system in cancer?

A

Role of immune system in cancer:

  1. Immunosurveillance- cancer prevention
  2. Immune cells DEVELOP into cancer cells
  3. Viruses- some can cause cancer
  4. Diagnosis (tumor antigens)
  5. Therapy.
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2
Q

Describe the current incidence of cancer in the world, using statistics. How many people die from the disease? What is the median age for cancer?

A

-20% of death in industrialized world is caused by cancer
-14 million new cases each year worldwide
-50% of people die from the disease (survival rates vary depending on type of cancer)
-Median age for cancer- 70 years old
-US- the lifetime probability of being diagnosed with cancer is 39.3% for men and 37.7% for women, which is a little more than 1 in 3.
Children have a genetic component for incidence in cancer.

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3
Q

What are some form of evidence that we have immune surveillance? What are methods used to kill tumors?

A

Evidence that we have immune surveillance mechanism (ex: immunosuppressed individual, hyper presence of skin cancer)
-Surgery, radiation, chemotherapy- “Slash, burn, poison”- all used to kill tumors.
lifestyle also contributes to cancer development.
more advanced cancer is , the less detected, harder to treat.

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4
Q

What is immune surveillance?

A

Immune surveillance- monitoring process of immune system to detect and destroy virally infected and neoplastically transformed cells.
evidence seen in mice, immunosuppressed individual with high incidence of tumors
-tissue dendritic cells induced to engulf foreign particles and undergo maturation and emigrate to afferent lymphatics to draining lymph node.

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5
Q

What is the second leading cause of death in the U.S. ?

A

CANCER is the second leading cause of death in the U.S in both men and women after Heart Disease (first)
22% of deaths in US in 2016 were from cancer.

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6
Q

what is a tumor/neoplasm?

A

Tumor/neoplasm- tissue in which cell are MULTIPLYING ABNORMALLY

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7
Q

What is a Benign tumor?

A

Benign tumor- ENCAPSULATED, LOCALIZED, Limited in size, and Rarely dangerous (warts)
-does NOT metastasize, not form cancer

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8
Q

What does Malignant mean?

A

Malignant- Can INVADE ADJACENT tissue

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9
Q

Define the term Cancer?

A

Cancer- Term to describe diseases caused by MALIGNANT tumors.

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10
Q

What is Metastasis?

A

Metastasis- the process by which MALIGNANT tumors SPREAD from the primary site to secondary site (may get in blood)
-most people die from mestasis.

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11
Q

Describe the two main solid tumors

A

Solid tumors:

  1. Carcinomas- EPITHELIAL cell orgin
  2. Sarcomas- CONNECTIVE tissue or NON-EPITHELIAL cell origin
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12
Q

What are the tumors of immune system?

A

Tumors of the immune system:
1.Leukemias: cancer of CIRCULATING cells
(cancer of blood)
-Lymphoid origin: acute lymphocyte leukemia (ALL), Chronic lymphocytic leukemia (CLL)
-Myeloid origin: acute myeloid leukemia (AML), chronic myeloid leukemia (CML)
2. Lymphomas: Cancer of LYMPHATIC TISSUE
-Hodgkin’s lymphoma: B cell origin- Reed Sternberg cells
-Non-Hodgkin’s lymphoma: (B and T cell origin)
3. Myelomas: Cancer of PLASMA cells

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13
Q

Further elaborate on Blood cancers.

A

Blood cancers:

  • Lymphomas: growth of lymphocytes in lymph node and Bone marrow. incidence of Hodgkin, non-Hodgkin lymphoma with > 100 subtypes
  • Multiple Myeloma: EXCESS PLASMA cells in Blood and bone marrow; cause bone lesions, kidney disease
  • Leukemias- Proliferation of circulating blood, bone marrow cells. have ACUTE (ALL (lymphatic), AML (myeloid), and CHRONIC (CLL (lymphatic), CML (myeloid leukemia), MPN (myeloproliferative neoplasms)
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14
Q

Where are the cancers located in the body of a male and female?

A

In males and females: Cancers can be lymph glands (lymphoma), Lung, pancreas, bladder, prostate, rectum, bone marrow (leukemia)
Cancers can be seen in skin (melanoma), breast, kidney, colon, ovary, uterus.

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15
Q

What are the necessary characteristics of cancer cells?

A

Necessary Characteristics of Cancer cells:
1. They stimulate their own growth
2. they ignore growth-inhibiting signals
3. They avoid death by apoptosis
4. They develop a blood supply: angiogenesis
5. They leave their site of origin to INVADE other tissues: mestasis
6. They replicate constantly to expand their numbers
7. they evade and outrun the immune response
cancer does NOT need ligand (bypass antigen signals)

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16
Q

what are the 10 Hallmarks of cancer?

A 
10 hallmarks of Cancer: 
1 .Sustaining proliferative signaling
2. Evading growth suppressions
3. Resisting cell death
4. enabling replicative immorality
5. inducing angiogenesis (form new blood vessels)
6. Activating invasion and metastasis
7. Deregulating cellular energetics
8. genome instability and mutation
9. *Avoiding Immune destruction
10 *Tumor-promoting inflammation
7-10 are NEW ones added
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17
Q

Further elaborate on components for 10 hallmarks of cancer. What makes each important?

A

10 hallmarks of Cancer:
1. Self sufficiency in growth signals
-Normal cells require growth cells to proliferate, but cancer cells ESCAPE this requirement (don’t need it)
2. Insensitivity to Antigrowth signals
-Normal tissues are protected from over proliferation by a variety of inhibitory signals, but cancer cells are INSENSITIVE to these signals
3. Apoptosis Evasion
-Apoptosis is used by normal cells to prevent damaged or defective cells from continuing to divide; apoptosis is INHBITED or Disrupted in cancer cells
4. Limitless Replicative Potential
-Normal cells have limited replicative potential due to telomere loss: cancer cells contain Active Telomerase (or other mechanisms) to maintain telomeres.
5. Sustained angiogenesis
-Tumor cells cannot grow beyond a few mm without a blood supply; cancer cells TRIGGER angiogenesis by activating genes encoding for angiogenesis stimulators and inhibiting genes encoding for angiogenesis inhibitors.
6.Tissue invasion and metastasis-
Cancer cells lose adhesiveness with neighbors, invade nearby tissues, and eventually metastasize around the body via circulatory system.
7. Deregulating cellular energetics
-Tumor cells are shown to reprogram cellular metabolism in order to support neoplastic proliferation.
8. Genome instability and mutation
increased mutability endows cancer cells with alterations that drive tumor progression.
9. Avoiding immune destruction
Evasion of immune system and destruction of cancer cells.
10. Tumor promoting inflammation
-It has shown that inflammatory responses can be tumor-promoting environments.

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18
Q

What must occur for cells to form cancer? What contributes to malignant transformation?

A

Cells must undergo MALIGNANT TRANSFORMATION to form cancer
Proto-oncogenes (normal RAS)- when MUTATED or MISEXPRESSED contribute to Malignant transformation (oncogene; mutant form)
TUMOR SUPPRESSOR genes- LOSS of function or expression contributes to malignant transformation.

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19
Q

What causes cancer?

A

Cancer are commonly caused by ENVIRONMENTAL agents and LIFESTYLE factors
Most of these factors act by TRIGGERING DNA MUTATIONS.

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20
Q

What form of data have allowed many causes of cancer to be identified? What kind of information is obtained?

A

EPIDEMIOLOGICAL DATA have allowed many causes of Cancer to be Identified

  • Epidemiology investigates the frequency and distribution of diseases in human population.
  • certain cancers are MORE Frequent in different parts of the world
  • To determine whether the causes are hereditary or environmental, scientists study RATES of Cancer in people Who have moved from one country to another.
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21
Q

Explain why environmental and lifestyle factors are mainly responsible for causing cancer.

A

Environmental and lifestyle factors are mainly responsible because:

  • People who move to new countries experience the same cancer rates as other inhabitants of the new country
  • This suggests that the most important factors in rates and types of cancer are environmental and lifestyle factors.
  • ex: most people who develop lung cancer: have a history of smoking cigarettes
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22
Q

Describe the correlation between smoking and cancer.

A

Smoking and cancer:

  • Heavier smokers develop cancer more FREQUENTLY than light smokers
  • Long-term smokers develop lung cancer MORE FREQEUNTLY than short-term smokers
  • Lung Cancer rates FALL for smokers who have quit smoking
  • Smoking is LINKED to many other types of cancer (bladder cancer, oral cancer ,esophagus)
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23
Q

Explain how many chemical can cause cancer.

A

Many chemicals can cause cancer, often after metabolic activation in the LIVER.
-Early observations of snuff users and chimney sweeps suggested that Exposure to certain chemicals was associated with Cancer.
-The list of known and suspected CARCINOGENS (cancer-causing agents) includes hundreds of chemicals.
-These chemicals do NOT always cause cancer by their own action, though.
repeated exposure to carcinogen causes disease.

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24
Q

How does acquiring new traits in tumor cells occur?

A

Acquiring New traits:
-New traits arise in tumor cells through additional DNA mutations, following original, initiating mutation
-New traits can be acquired through EPIGENTIC MECHANISMS as well.
Epigenetic mechanisms- the INHBITION of Gene function WITHOUT mutating DNA sequence.

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25
Q

Explain how Viruses and other agents trigger development of cancers. Who discovered this and how did he do it?

A

Viruses and other Infectious agents trigger Development of Some Cancers:

  • in 1911, Peyton Rous first demonstrated that cancer can be caused by Virus
  • the chickens he studied has SARCOMAS (cancers of Connective tissue)
  • He ground tumor tissue and passed it through a filter that even bacteria could NOT pass through; the extract caused cancer when injected in healthy individuals.
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26
Q

What percent of cancers are viruses associated with? Describe the DNA and RNA viruses that associated with human cancers.

A

Viruses are associated with 15% of Human cancers
DNA viruses:
1. Papillomavirus (many distinct strains; HPV)- associated with Genital warts (BENIGN Tumors) and Carcinoma of uterine Cervix ; seen worldwide
2. Hepatitis B virus- associated with LIVER cancer (hepatocellular carcinoma); mainly seen in southeast Asia/Africa
3. Epstein Barr virus- associated with Burkitt’s lymphoma (cancer of B lymphocytes) and Nasopharyngeal carcinoma (seen in West Africa, immunosuppressed individuals)

RNA Viruses:
1. Human T-cell Leukemia virus type 1 (HTLV-1) associated with adult t-cell Leukemia / lymphoma (seen in Japan, west indies)

  1. Human immunodeficiency virus (HIV-1) and Human Herpesvirus 8 (HHV8) associated with Kaposi’s sarcoma. Highly seen in Central Africa
27
Q

Describe what the immunosurveilance theory says.

Also discuss how long one can recognize tumor and how immune system may react.

A

Immuneosurveillance Theory- postulates that immune destruction of cancer cells is Common, and cancer results from an occasional failure of the immune system to destroy the aberrant cells.
many years can go by without patient or immune system recognizing tumor.
-Tissue damage from growth may eventually trigger the immune system (inflammation)- sometimes too late.

28
Q

Describe incidence of breast cancer in terms of diameter of tumor and tumor cell population.

A

Growth of a breast cancer:
As tumor cell population doublings increase, you get LARGER diameter of tumor.
Tumor is first visible on x-ray with 10^8 cells
-Tumor first palpable with 10^9 cells (visible and tangible)
-Death a patient occurs with 10^12

29
Q

Elaborate on some early evidence supporting immunosurveillance

A

Early evidence supporting immunosurveillance:

  • some cancer patients that contracted bacterial infections experienced regression of tumors
  • BCG Vaccine (mycobacterium bovis treatment) for superficial Bladder cancer- showed chronic inflammation of the bladder (meaning immune system induced)
  • Organ transplant patients, who take immunosuppressive drugs, develop cancers at HIGHER rates than normal.
30
Q

Explain how tumors can grow in some mice and not in other mice. Also discuss how same concept occurs in humans. what recognizes allogenic MHC I molecules?

A 
Tumors can be transplanted into mice with IDENTICAL MHC type and FAIL to grow in mice with DIFFERENT MHC type. 
Allogenic MHC class I molecules are recognized by Alloreactive CD8 T cells. 
same results seen in humans- for transplantation, cancer stem cells, barrier preventing spread of tumor cells from person to person.
31
Q

Describe the experiment of mice with tumor cells , depending on MHC type.

A

experiment:

  1. Tumor cells isolated from primary tumor in MHC a mouse
  2. Tumor cells from MHCa mouse injected into other MHCa mouse which causes tumor to grow and animal dies
  3. Tumor cells from MHCa mouse injected into MHCb, tumor is REJECTED and animal lives.
32
Q

What are tumor antigens?

A

Tumor antigens: antigen to which the immune system responds

33
Q

Differentiate between tumor specific antigens and tumor associated antigens?

A

Tumor Specific antigens: antigens present ONLY on Tumor cells
-Viral proteins
-mutated portion of cellular protein
-protein portions generated from recombination between genes
-Abnormal protein modification patterns
-peptide slicing
Tumor Associated antigens: antigens expressed on BOTH NORMAL and TUMOR cells. Usually smaller amounts on normal cells.

34
Q

further elaborate on mechanism of tumor specific antigen and tumor associated antigens.

A
  1. Peptide antigen presented on MHC class I on normal cells, and cells undergo mutation and becomes cancerous
  2. Presentation of mutant peptide from mutated cellular protein leads to formation of tumor specific antigen
  3. reactivation of embryonic genes not normally expressed in differentiated cells AND Overexpression of self protein by a tumor increases self-peptide presentation and recognition of T cells, creating tumor-associated antigens.
    peptide antigens composed of different amino acids.
35
Q

What is the Bcr-Abl Translocation and CML?

A

Chronic Myeloid Leukemia (CML) is caused by a Bcr-Abl Translocation
This translocation- is rearrangement of genetic material between chromosome 9 and chromosome 22.
Bcr gene from chromosome 22 will FUSE with Abl gene from chromosome 9. This creates abnormal fusion Bcr-Abl that is on Philadelphia chromosome.
The Bcr-Ab1 gene causes CML cells to grow and reproduce out of control

36
Q

Describe what occurs in peptide splicing.

A

Peptide splicing:

  1. Two noncontiguous peptides within the melanocyte glycoprotein gp100 are cut out and spliced together in proteasome
  2. Spliced gp100 peptide is presented by HLA-A*32 and recognized as NOT self by the patient’s CD8 T cells.
37
Q

Explain how successful tumors develop the ability to evade immune system. What increases likelihood of acquiring this ability?

A

Successful tumors develop the ability to EVADE immune system.

  1. Tumor cells have increased MIC expression (MHC I truncated genes)
  2. NKG2D on NK cells and gamma:delta T cells bind MIC: the tumor cells are killed
  3. variant tumor cell cleaves MIC from its cells surface. Soluble MIC then binds to NKG2D on lymphocytes.
  4. Variant tumor cell is NOT killed and survives to proliferate and cause cancer.
    * As tune goes on, acquired mutation increases likelihood that tumor cell will acquire this ability.
38
Q

What happens when there is a loss of HLA class I molecules?

A

Loss of HLA class I molecules- Cancer cells STOP EXPRESSING- won’t present antigen cytotoxic CD8 T cells- 1/3 to 1/2 of tumors.

39
Q

what happens when there is a tumor-induced suppression of immune response? what is the clinical outcome? What leads to a better prognosis of cancer?

A

In the absence of inflammation, NO B7 costimulators- T cell becomes ANERGIC (lack of reaction by body’s defenses to foreign particle)
some tumors secrete ANTI-INFLAMMATORY Cytokines- immunosuppressive environment- recruit Tregs (t regulatory cells)
Clinical outcome: increased number of Tregs in tumor, POORER PROGNOSIS
Increased number of Cytotoxic T-cells, TFH cells, memory T cells and B-cells, the BETTER the prognosis.

40
Q

Describe the components of HPV (human papillomavirus). what components of HPV can inactivate tumor suppressor genes?

A

HPV-human papillomavirus:
-Sexually transmitted- 50% of sexually active people INFECTED- can cause anal, mouth and throat cancer
-Integrated HPV DNA into human genome- viral genes (E6, E7) can INACTIVATE TUMOR SUPPRESSOR genes (prB, and P53)
100 different types of HPV, 30 can infect genitalia- some cause genital warts, others cause cancer.

41
Q

How are antibodies made toward HPV? what are components of HPV vaccine?

A

Antibody is made toward Variable region of L1 protein- viral caspid
HPV vaccine- recombinant L1 protein- non-infectious particles that resemble virus
Routine vaccination began in 2006- girls (13-21), boys (11-26)
HPV vaccine required before becoming sexually active

42
Q

What are all the papillomavirus proteins and their functions?

A

Papillomavirus proteins:
L1- MAJOR capsid protein
L2- minor capsid
E1- DNA helicase
E2- Transcription factor
E4- structural protein expressed by Infected Keratinocytes
E5- Cofactor for epidermal growth factor, regulates MHC class I expression
E6- p53 degradation, telomerase activation
E7- binding to Rb, E2F release.

43
Q

Compare and contrast the different Human papillomavirus vaccines

A 
Human papillomavirus vaccines:
Bivalent vaccine- Cervarix (2009)
-Tetravalent/quadrivalent vaccine -Gardisil (2009)
9- valent vaccine- Gardasil 9 (2014)
Boys- tetravealent
Girls- do bivalent/tetravalent vaccine
44
Q

Differentiate between bivalent vaccine and tetravalent vaccine.

A

Bivalent vaccine: HPV 16, HPV18, adjuvant: aluminum hydroxide and protection: 70% of cervical cancers
Tetravalent vaccine: HPV16, HPV18, HPV6, HPV11; adjuvant: amorphous hydroxysulfate and protection:70% of cervical cancers and 90% of genital warts

45
Q

Elaborate on Bivalent vaccine, and its composed and who are allowed to receive it. Which HPV forms cause cervical cancers

A

HPV16, 18- cause 70% of cervical cancers
Bivalent vaccine- also contains ENDOTOXIN (bacterial cell-wall lipopolysaccharide)
this vaccine admnistered for females only.
quadrivalent/9valent vaccine seen in females and males.

46
Q

What are the cancer vaccines? what is the result of patient vaccinated?

A

Cancer vaccines:
CT antigen: MAGEA1 and MAGEA3 (melanoma antigen encoding)
used to try and create immune response and attack melanoma
patient vaccinated 11 times over 2 years with MAGEA3 (recombinant viral vaccine and synthetic peptide)
-Only 20% regression (decrease in size of tumor), and 10% remission (signs and symptoms reduce)- perhaps vaccine specific T regs.
trial did not work together.

47
Q

What occurs in melanoma? describe role of CTLA4 and its antibody? what are side effects?

A

Melanoma- immune response is TOO WEAK- enhanced by increasing Co-stimulatory signal (antiCTLA4 antibody) (ipilimumab)
CTLA4 competes with CD28 for B7- antibody SEQUESTERS CTLA4 (prevent it from binding B7)
Side effects: Increased INFLAMMATION and Lowered threshold for T-cell activation-diarrhea, colitis, and skin rashes.

48
Q

Describe what happens in T-cell activation, inhibition and persistent T cell activation in relation to CTLA4, CD28.

A
  1. signals from the T-cell receptor and CD28 co-stimulatory receptor lead to t-cell activation
  2. B7 is preferentially bound by CTLA4 and no longer engages CD28; so T-cell is inhibited
  3. ANTI-CTLA4 antibody BLOCKS the binding of CTLA4 to CD28 and leads to PERSISTENT T-cell activation
49
Q

Explain what occurs in Adoptive T cell transfer and how one can mutagenize low-affinity receptors from patients.

A 
Adoptive T-cell transfer- ISOLATE tumor tissue from patient and culture in vitro with IL-2 (activated T-cells that have infiltrated tumor tissue); observe which cultures result in melanoma cell death; expand and reinfuse activated T-cells
you can also mutgenize LOW-AFFINITY receptors from patients- cells can Still DOWNREGULATE HLA Class I, is restricted to HLA class I allotype.
50
Q

What increases CD4 and CD8 T cell response? Describe the process. What components prevent anergy?

A

Chimeric antigen receptors (CAR) used to INCREASE CD4 and CD8 T cell response.
Antigen binding site made from the heavy chain and light chain variable domains of an antibody (Fv-variable fragment)
Cytoplasmic tail contains signaling domains from TCR, another activating receptor (ex: CD137) and CD28 co-receptor prevents ANERGY- high affinity like IgG.
they express chimeric receptor in patient T-cells then put back in patient (CAR T cells)

51
Q

What is used for treating B cell tumors?

A

ANTI-CD19 chimeric antigen receptor used for treatment of B-cell tumors (also expressed on follicular dendritic cells)
CAR T cell kills B-tumor cell

52
Q

What is an example of anti-CTLA4 antibody therapy? how does it work?

A

IPILIMUMAB- example of anti CTLA4 antibody therapy- checkpoint inhibitor that inhibits the physiological process that limits the strength of T-cell activation pathway.

53
Q

What occurs in adoptive Transfer of Antigen-activated dendritic cells? Explain the process

A

Adoptive Transfer of Antigen-activated dendritic cells- you isolate patient monocytes, and expose to antigen in vitro and transfer back to patient.

mechanism:
1. Monocytes isolated from prostate cancer patient, and are cultured with a fusion protein of GM-CSF and prostatic acid phosphatase (PAP)
2. GM-CSF induces the monocytes to mature into dendritic cells. PAP is internalized with GM-CSF and is processed into peptides that are presented by MHC class II.
3. The activated dendritic cells are induced into patient, where they travel to the spleen and present PAP antigens to naive T cells.

54
Q

What occurs in Late-stage metastatic prostate cancer?

A

Late stage metastatic prostate cancer- cells cultured with PAP-GMCSF fusion protein. GM-CSF binds to protein, internalized, differentiates to dendritic cell. PAP is then processed in endosome and presented on MHC class II- antigen-primed monocytes- this is first example of FDA approved cancer vaccine

55
Q

describe how monoclonal antibodies affect cell surface antigens. How does the killing occur?

A

Monoclonal antibodies to cell surface antigens:
antibodies to cell surface molecules- “naked” or conjugated to toxin or radioactive isotope (immunotoxins)
-Killing by NK cells or opsonization (complement fixation and phagocytosis) or by conjugated toxin

56
Q

How are monoclonal antibodies useful for cancer detection?

A

Monoclonal antibodies for Cancer detection:
-cause IMPROVED precision in detecting tumors- distinguish closely related tumors.
-Ex: B-cell tumors originating from different stages of development
IGH- large polypeptide subunit of antibody.

57
Q

Describe what is seen in Burkitt’s lymphoma

A

Burkitt’s lymphoma-
cell: hematoxylin and eosin stain
gene- DNA hybridization with anti-MYC oncogene probe
protein- Anti-MYC oncoprotein antibody

58
Q

Describe what is seen in Hodgkin’s lymphoma

A

Hodgkin’s lymphoma-
Hematoxlin and eosin stain (owl eyes)
ANTI-PAXS antibody (loss of Pax 5 expression)
-Anti-CD30 antibody (expression of CD30
anti-CD15 antibody (expression of CD15)
expression of CD30 and CD15 indicate Hodgkins disease.

59
Q

Explain the antibody produced in Hodgkin’s lymphoma.

A

Hodgkin’s lymphoma- BRENTUXIMAB-VEdotin CONJUGATE
anti-CD30 antibody (brentuximab) conjugated to linker and cytotoxic drug (auristatin)
*targeted toward tumor cell
mechanism:
1.AntiCD30 is conjugated to auristatin by a cathepsin-cleavable linker
2. Conjugate binds to CD30 and is internalized by lymphoma cell. Conjugate is cleaved into the endosomes by cathepsin. Auristatin enters the nucleus and binds microtubules.
3. lymphoma cell cannot form a mitotic spindle and is unable to divide and dies by apoptosis.

60
Q

Describe the antibody produced in NON-Hodgkin’s lymphoma and mechanism involved.

A

Non-Hodgkin’s lymphoma- Ibritumomab
Anti-CD20 antibody conjugated to radioactive isotope.
Radiation is directed at SURFACE of tumor instead having to pass through tissue.
mechanism:
1. Anti-CD20 conjugated to radionuclide
2. Radioactive antibody binds to the malignant b cells and irradiates them
3.The radiation damages the cells’ DNA and kills them.

61
Q

Differentiate between the gamma radiation and beta radiation used in Non-Hodgkin’s lymphoma.

A

Indium-111 isotope- target and image tumor (gamma radiation)
Yttium-90- targets for KILLING (beta-radiation)
-radiation is directed at surface of tumor instead of having to pass through tissue.

62
Q

what is the purpose of antibody-dependent cellular cytotoxicity (ADCC)

A

Antibody-dependent cellular cytotoxicity (ADCC)- use of therapeutic monoclonal antibodies to kill tumor cells- NK MEDIATED
Therapeutic antibodies are Specific for protein on surface of tumor cells.

63
Q

What cell structures interact that indicate losing battel against tumor. what is the result of this? what can lead to autoimmunity?

A

Continued engagement of PD-1 on T cells with PD-L1 tumor cells leads to T-cell exhaustion- sign LOSING battle against the tumor- Leads to progressive LOSS of Effector function, gene expression and Metabolic changes.
PD- 1 on tumor cells suppresses tumor-killing activity of t cells
PD-L1 antibody - monoclonal antibody against program cell death. (helps keep body’s immune defenses under control)
checkpoint inhibitors can lead to autoimmunity.

Systems Physiology (19 decks)

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