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Immunity-PROF Question Flashcards

1
Q

which graft rejection beshi ??

A

xenograft

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2
Q

why xenograft beshi rejected ?

A

HLA type mile na

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3
Q

SOMC te ki ki transplant hoy ?

A

cornea

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4
Q

HLA nam keno hoise <

A

first human e dekha jay

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4
Q

antigen defination ?

A

any substance that can be recognized
by the Ig receptor of B cell / by the T cell when complex with MHC

350

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5
Q

hypersensitivity 1 which Ig mediated ?

A

IgE

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5
Q

Cochelar transplant e ki transplant hoy ?

A

surgical implementation
a samll electronic device that directly stimulates the auditory nerve in the inner ear to produce a sense of sound

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6
Q

IgG er subtype koyta ?

A

4

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7
Q

IgA er subtype koyta ?

A

2

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8
Q

duration of type 1 H >

A

immediate

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9
Q

duration of Type4 H >

A

delayed

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10
Q

amra je oramenta pori- er theke scratch khaile kon hypersensitivity?

A

type=-1

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11
Q

ar ki ki type =1 H ?

A

375

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12
Q

which AB fix complement ?

A

IgG
IgM

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13
Q

complement fix krte pare na kon AB<

A

ig - A E

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13
Q

Type-2 H ?

A

388

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13
Q

is tuberculin test specific ?

A

no
low specificty

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13
Q

Directly complement fix kore ?

A

Igโ€“G M

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13
Q

immunodeficiency D kon age hoy >

A

old age

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14
Q

kon AB kon type er Hypersensitivity kore?

A

IgE = 1
IgG = 2 3

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14
Q

kon type4 hypersensitivity test amra commonly kori >

A

tuberculin test

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14
Q

why old age e immunodeficiency diseases ?

A

regulatory T cell function weak
dec tolerance

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14
Q

primary & secondary immune response >

A

341

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15
Q

procedure of tuberculin test ?

A

5TU - tuberculin unit = 0.1 ml
intra-dermally on the flexor aspect of the forearm
observed half an hour - 30 min for - immediate hypersensitivity
2 hr por final reading

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15
Q

H - 1 2 3 ki mediated <

A

immune mediated
juts 4 = cell mediated

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16
Q

B cell origin <

A

stem cells of Bone amrrow

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16
Q

HELPER T cell type ?

A

Th1
Th2

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16
Q

type-4 h ki mediated ?

A

cell

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16
Q

body te B cell beshi naki T cell <

A

T cell
60-70%

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16
Q

maturation of B cell site <

A

bone marrow

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16
Q

origin of T cell <

A

bone marrow stem cells

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16
Q

maturation of T cell ,

A

thymus & GALT

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16
Q

which immunosuppressive in COVID >`

A

corticosteroids
IL-6 inhibitors - tocilizumab

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16
Q

Th1 fucntion ??

389

A

secreted IFN-gamma
delayed hypersensitivity
IFN gamma - activate macrophage

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17
Q

RF e kotodin por Ab-Atg produce hoy ?

A

2-3 weeks

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18
Q

RF e kar against a AB produce hoy ?

A

streptococcal Atg

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19
Q

Ki ki host tissue ache ,

A

heart valve glycoprotein
myocardial sarcolema
cardiac myosin
neuronal Ab in sub-thalamic and caudate nuclei

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20
Q

Rheumatic fever er primary infection ?

A

pharyngitis / sore throat by streptoccocus

168

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21
Q

RF type of hypersensitivity?

A

Type=2

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22
Q

Which AB in breast milk ,

A

IgA

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23
Q

Placenta cross kore kon AB <

A

IgG

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23
Q

anaphalaxis hole ki korba >

A

desensitization

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24
Q

IgE fucntion ,

A

immediate hypersensitivity
defend parasitic infections by casuing release of enzymes from eosinophils

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25
Q

desensitization ,

A

379

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26
Q

what is hapten ?

A

353

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26
Q

mediators of anaphylaxis?

A

378

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27
Q

which cells in anaphylaxis ,.

jhuma mam

A

378

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28
Q

Vaccine dile kon immunity ?

A

acquired
active artificial

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28
Q

type-4 H M/A ?

A

389

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29
Q

B cell fucntion ,

A

336

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30
Q

Which Ig is secretory?

A

IgA

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31
Q

immunoglobulins dile kon immunity <

A

passive

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32
Q

MHC & HLA ki same <

A

YES

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32
Q

MHC & HLA full form <

A

major histocompatibilty complex
human leukocyte antigen

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33
Q

differnce ki HLA & MHC ER <

A

MHC - Protein - cluster on gene
HLA - gene
HLA - MHC in human

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34
Q

MHC - 1 & 2 fucntion ,

A

372

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35
Q

RF in immunology must fro Jhuma mam >

A

168

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36
Q

antibody type <

A

GAMED

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37
Q

Sobceye beshi kon AB <

A

IgG - 75%

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38
Q

Ig kon dhoroner immnuty dey ?

A

PASSIVE

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38
Q

Molecular mimicry example .

A

GBSโ€™
reitres syndrome
R heart d

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38
Q

kom AB konta ?

A

IgE
0.004%

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39
Q

first time AB dhukle kon complement /

A

Alternative

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40
Q

Complement prokash kori ki diye

A

C

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41
Q

Immunodeficiency disease ki <

A

Defects in one or more components of the immune system can lead to seriuous and often fatal disorders
that are ccollectivly known as โ€“

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41
Q

immunologically previleged sites >

A

brain
eyes
testes
ovary

joint cartilage
immune response are limited

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41
Q

T cell type <

A

CD4+
CD8+

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42
Q

Complement kon type protein ,

A

Plasma

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43
Q

Importance of MHC ?

A

372

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43
Q

3 difference between sensitization and de-sensitization ?

A

Here are three key differences between sensitization and de-sensitization:

  1. Immune Response:
    • Sensitization: The immune system develops an increased sensitivity to an antigen, often leading to an allergic or hypersensitivity reaction upon subsequent exposure.
    • De-sensitization: The immune system is gradually exposed to an allergen in controlled doses to reduce or eliminate hypersensitivity reactions.
  2. Outcome:
    • Sensitization: Results in heightened immune reactivity (e.g., IgE production in allergies).
    • De-sensitization: Aims to induce immune tolerance, reducing or preventing allergic reactions.
  3. Clinical Application:
    • Sensitization: Often undesirable, as it underlies conditions like allergies, asthma, or transplant rejection.
    • De-sensitization: Used therapeutically to treat allergies (e.g., immunotherapy) or prevent reactions to medications (e.g., penicillin de-sensitization).
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43
Q

MHC-1 vs 2 ?

A

372

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44
Q

what is Minor-histo compatibility complex <

A

The minor histocompatibility complex refers to a group of antigens encoded by genes outside the major histocompatibility complex (MHC). These antigens can trigger an immune response during organ or tissue transplantation, even when the donor and recipient are MHC-matched. They are called โ€œminorโ€ because they elicit weaker immune responses compared to MHC antigens, but they can still contribute to graft rejection or graft-versus-host disease (GVHD).

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45
Q

cytotoxic T cell receptor ,

A

TCR
CD 8

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46
Q

Immunology def >< Jhuma mam

A

325

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47
Q

immunocompotent cell er name <

A

332

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48
Q

APC example ?

A

332

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48
Q

AB production M/A ?

A

345 whole figureee

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49
Q

graft /

A

392

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50
Q

ekta baccha congenital anomely niye jonmale ki valo kichu hobe ?>

A

NO

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50
Q

keno valo hobe na .

A

kichu din por por infection hobe

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51
Q

kivabe eii baccha ke safe rakhba ? H

A

hygiene maintain
relatives niye beshi vir kora jabe na

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51
Q

ICT te stool niye ki dekhbo ?

A

Atg blood e dekhbo AB

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52
Q

a bacteria and virus that have both live and kille dvaccine ?

A

V Cholerae
Polio

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52
Q

Why NK cells called so ?

A

338

they activate without prior exposure to the virus

not enhanced by exposure

not specific for any virus

kill without AB
no need of MHC

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53
Q

HOW NK cell then kill virus <

A

perforins โ€˜granzymes

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54
Q

Graft er age ki ki mesaure <

A

397

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55
Q

fate of graft ?

A

acceptsnce

or rejection

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56
Q

tumor immunity mechanism ,

A

400
must

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57
Q

is blood transfusion is called transplantation ??

A

Blood transfusion is not called transplantation because it involves the transfer of only blood or blood components (e.g., RBCs, plasma) rather than solid organs or tissues. Transplantation typically refers to the grafting of organs, tissues, or cells (e.g., kidney, bone marrow) that integrate into the recipientโ€™s body. Blood transfusions are temporary and do not involve long-term engraftment.

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57
Q

test done before blood donation ?

A
  1. Donor Questionnaire
  2. Hemoglobin/Hematocrit Test
  3. Blood Typing (ABO and Rh)
  4. Infectious Disease Screening (e.g., HIV, Hepatitis B/C, Syphilis)
  5. Blood Pressure Check
  6. Pulse Rate Check
  7. Temperature Check
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58
Q

cross matching e blood na mille shei blood dile ki hobe >??

A
  1. Acute Hemolytic Reaction
  2. Disseminated Intravascular Coagulation (DIC)
  3. Renal Failure
  4. Hypotension and Shock
  5. Jaundice
  6. Anaphylactic Reaction
  7. Death
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59
Q

cause of hyperacute graft rejection ?

A

Hyperacute rejection is characterized by thrombotic occlusion of the graft vasculature that begins within minutes to hours after host blood vessels are anastomose to graft vessles and mediated by pre-existing AB and the host circualtion

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60
Q

which Ig in primary response >

A

IgM

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61
Q

Which AB in secondary response?

A

IgG

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62
Q

Cell mediated immunity component ?

A

innate
=NK cell
=macrophage

adaptive
=Th
=Tcyt

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63
Q

humoral immunity component >

A

innate
=neutrophil
=complement

adaptive
=B cell
=plasma cell

328

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64
Q

desensitization type >

A

acute
chronic

65
Q

acute desensitization kivabe <

A

very small amout of Atg at 15 minutes intervels

66
Q

cchronic desensitization?

A

long term administration weekly

67
Q

IgA destroy kore emon baccteeria er criteria ki ?

A

capsulated

68
Q

emon bacteria er example deo&raquo_space;

A

Some capsulated bacteria that can produce IgA proteases (enzymes that destroy IgA) include:

  1. Streptococcus pneumoniae
  2. Haemophilus influenzae
  3. Neisseria meningitidis
  4. Neisseria gonorrhoeae

These bacteria use IgA proteases to evade mucosal immune defenses.

69
Q

site of secretory IgA ?

A

Secretory IgA (sIgA) is primarily found at mucosal surfaces, including:

  1. Gastrointestinal tract
  2. Respiratory tract
  3. Genitourinary tract
  4. Saliva
  5. Tears
  6. Breast milk

It plays a key role in mucosal immunity by preventing pathogen attachment and invasion.

70
Q

Splenectomy pt e jeno capsulated bacteria disease korte na pre tar jonno ki korbo ?

A

vaccination

71
Q

site of destruction of capsulated bacetia >?

72
Q

why fetus as an allograft
not rejected ?

A

trophoblast layer

73
Q

Thymic educationn ?/

74
Q

hybridoma ki ?

A

b cell + myeloma
fusion derived immortalized
AB producing cell

75
Q

which monoclonal AB in rheumatoid arthirits >

A

infliximab
adalimunab
rituximab
certolizumab

76
Q

which AB has no AB-like function ?

76
Q

Kon AB er molecular weight beshi ?

76
Q

why IgG can pass placenta ? i

A

its Fc portion can bind with placental membrane

77
Q

then what is the fucntion of IgD ><

78
Q

monoclonal Ab ki >

79
Q

PENTAMAR konta <

80
Q

monomar ke M

81
Q

B cell maturation ??

A

335
stemcell โ€” pre B cell โ€”- B cell immature โ€“ mature โ€“ activated โ€“ plasma cell

82
Q

Th 1 2 fucntion ,

83
Q

MAC ki kore <

A

cell lysis

84
Q

ultimate product of complement >

85
Q

helper T cell fucntion ?
valo kore bolte hobe

86
Q

T cell release cytokine <

A

IL-2
TNF
IFN- gamma

87
Q

Agglutination VS precipitation ..

88
Q

IgM form >

A

monomaric
pentamaric

89
Q

First which AB is produced in body ,

90
Q

what is prozone phenomenon ?

A

inhibition of agglutination by excess AB

91
Q

How to overcome prozone phenomenon ?

A

AB dilution kore

92
Q

Latent TB er shomoy ki korbo ?

93
Q

which type is Th17 cell <

A

CD4+ helper cell

94
Q

source of complement ?

A

liver
macrrophage
fibroblast

365

95
Q

Function of IgM ?

A

primary response
fix compliment

96
Q

Type-1 2 3 hypersensitivyt ki mediated ,

97
Q

normally complement kemon thake >

A

plasma te inactiavte thake

98
Q

vaccine dile kivabe AB produce hoy ?

99
Q

CMI te participate kore na ke?>
B /T ??

100
Q

T cell VS B cell ,

101
Q

epitope spreading ki /

102
Q

active passive example /

103
Q

3 ta complement pathway kokhon ek jaygay asbe .

A

C5 produce er shomoy

104
Q

which one is central complement >,

105
Q

activator of complement >

106
Q

immunodeficeincy te complement deficiency hole ki hobe ?

A

C3b โ€“ jhuma mam
pyogenic bacterial infection

107
Q

why name B cell <

A

they first discovered in birds
where maturation occur in bursa of Fabricus , a lympho-epithelial organ in birds

108
Q

T cell why this name <

A

mature and develop in the thymus gland

109
Q

widal test type ?

A

serological

110
Q

atopy example <

A

urticaria
allergic rhinits
bronchial asthma
angioedema
eczema

111
Q

SOMC te kon kon transplantation ?

A

cochlear
liver
kidney
cornea
heart
cartilage

112
Q

why IgE IN type- 1 ?

113
Q

paralysis type in GBS >

114
Q

polio vs GBS <

A

Paralysis pattern
polio - asymmetrical
GBS - symmetrical + ascending

115
Q

GBS kivabe hoy /

A

Compylobacter diye

116
Q

main fucntion of AB ,

A

recognize and bind to foreign sundtances

117
Q

antigen er MW kom hole problem ki <

A

weak immunogenic

118
Q

which immunity exercise korle bare <

119
Q

MW of antigen >

A

> 10K dalton

120
Q

systemic immune complex disease in Type-3

A

AB-Atg complex deposition in circulation

121
Q

localized type of type-3 H ,

A

glomerulonephritis
arthirits

122
Q

Type-3 hypersensitivity type ?

A

systemic
localized

123
Q

what is CD <

A

Cluster differentiation

124
Q

acute infection which AB <>

125
Q

CHronic infection which AB <

126
Q

PHYSIOLOGIC sequlae of immunodeficeincy disease <

A

general malnutrition
energy metabolism
trace metal deficiency
vitamin deficeincy

127
Q

which monoclonal AB in cancer <

A

bevacizumab
cetuximab
panitumumab

128
Q

ICT kit ki type type /

129
Q

principle of ICT /

A

rapid strip based immunoassay
qualitiative

130
Q

CFT example

A

kala azar
gonococcus
filatiaisi

131
Q

slide agglutination >

A

serotyping of bacteria
blood grouping

132
Q

latex <

A

HBsAg detection
ASO titer

133
Q

tube <

A

widal test
weil felix test

134
Q

IF /

A

detect T B cell

135
Q

secondarybB ce;ll

A

hypogmmaglobulnemia
dec sy theiss of IgG

136
Q

primary T cell deficiency ,

A

thymic aplasia
hyper-IgM syndrome
chronic mucocutanueous candiditis

137
Q

primary B cell deficeincy >

A

Ig deficiency
X linked Brutons hypogammaglobulinemia

138
Q

Secondary T cell

A

AIDS โ€˜
HIV
measles

3.38PM
13-2-2025

139
Q

how IgG pass placenta ?

A

neonatal Fc receptor FcRn located on the syncytotrophoblast of the placenta

140
Q

properties of IgG ?

A

Monomar
blood + interstitial fluyid
secondary response
fix complement
enhance complement

141
Q

type-2 Hypersensitivity name ?

A

cytotoxic mediated

142
Q

which IL produce CRP ?

143
Q

Protein of immune system ?

A

CRP
MBP
lipopolysaccharide

144
Q

RF kon type ?

145
Q

AGN kon type ?

146
Q

eye e kon immune component ?

147
Q

acute phase protein name ?

A

CRP
alpha 1 anti-trypsin
alpha 2 macroglobulin
C9
factor B
fibrinogen

148
Q

chemical classify of Atg ?

A

protein
lipid
NA
polysaccharide

149
Q

which Atg most potent ?

150
Q

cytotoxic cell konta ke kill kore /

A

tumor cell
graft cell
virus infected cell

151
Q

plasma cell theeke ki toiri ?

152
Q

B cell to plasma hote ki lage ?

153
Q

Complement deficinecny whicch N ?

A

N meningitis

154
Q

beshi AB ?

155
Q

2nd beshi AB ?

156
Q

primary vs secondary immune response ?

157
Q

NK dekhte kemon ?

A

granular large lymphpcyte

158
Q

shape of immunoglobulins ?

159
Q

portion koyta ?

160
Q

Fc portion why ?

A

portion of carboxyl terminal
fraction crytallized

161
Q

Fab portion why ?

A

antigen bind

162
Q

merits and demerits of immune response ?

163
Q

why no immune response in spermatic cord ?

A

Blood testis barrier
fas ligand - induce apoptosis
testestorione -suprress immune activation

164
Q

immunity def ?

A

all those physiological mechanism
that endow the individual
with the ability to
recognize materials foreign to itself
and to neutrilize
metabolize / eliminbate it
with / without injury to the host cell

165
Q

functions of innate immunity ?

A

killing invading microbes
activating adaptive immunity

mam slide

166
Q

in which case penicillin IV ?

A

bacterial meningitis
neurosyphillis
gas gangrene
anthrax

167
Q

which test before this ?

A

skin test
gram stain
sensitivity test

168
Q

immunodeficeiy disorder example must ?

169
Q

erytrhoblastosis fetalis ??

A

๐Ÿ‘ถ๐Ÿ”ด Erythroblastosis Fetalis (Hemolytic Disease of the Newborn)
- Cause: Maternal IgG Abs against fetal RBC Ags (Rh incompatibility, ABO less severe).
- Pathophys: Rhโป mother โŸถ Rhโบ fetus โŸถ sensitization (1st pregnancy) โŸถ IgG anti-D Abs cross placenta (2nd pregnancy) โŸถ fetal RBC hemolysis.
- Sx: Hydrops fetalis, anemia, jaundice (โ†‘unconj. bilirubin), hepatosplenomegaly, kernicterus.
- Dx: Coombs test (Direct + on newborn RBCs).
- Tx: Exchange transfusion.
- Prevention: RhoGAM (Anti-D Ig at 28wks + postpartum).

@usmlereviews

170
Q

coombs test all

171
Q

why preganancy immunodeficiency state

A

๐Ÿคฐ๐Ÿ“‰ Pregnancy = Immunodeficient State
- ๐Ÿ”ปTh1, ๐Ÿ”บTh2, ๐Ÿ”บTregs โŸถ โ†“cell-mediated immunity.
- Hormones: โ†‘Progesterone, Estrogen, hCG, Cortisol โŸถ immunosuppression.
- Placenta: No MHC-I (syncytiotrophoblast), HLA-G โŸถ NK cell inhibition.
- Effect: โ†‘Infections (Listeria, CMV), โ†“Autoimmune flares (RA).

@usmlereviews

172
Q

example of immunodeficient state ?

A

๐Ÿฆ ๐Ÿ“‰ Examples of Immunodeficient States

  1. Primary (Congenital)
    • X-linked Agammaglobulinemia (BTK mut โŸถ โ›” B cells)
    • SCID (Adenosine deaminase def, IL-2Rฮณ mut โŸถ โ›” T/B cells)
    • Hyper-IgM Syndrome (CD40L defect โŸถ โ›” class switching)
    • DiGeorge Syndrome (22q11 del โŸถ โ›” T cells, thymic aplasia)
  2. Secondary (Acquired)
    • HIV/AIDS (CD4+ T cell depletion)
    • Chemo/Radiation (BM suppression)
    • Pregnancy (Th1 โฌ‡, Th2 โฌ†)
    • Diabetes (Neutrophil dysfunction)
    • Malnutrition (Zinc, protein def โŸถ T cell impairment)

@usmlereviews

173
Q

which vaccine form part of a bacteria ?

A

๐Ÿฆ ๐Ÿ’‰ Subunit (Component-Based) Bacterial Vaccines

  1. Toxoid Vaccines (Inactivated bacterial toxin)
    • Diphtheria (Corynebacterium diphtheriae)
    • Tetanus (Clostridium tetani)
  2. Polysaccharide Vaccines (Capsular Ag, ยฑ conjugation for T-cell response)
    • Pneumococcal (Strep. pneumoniae) (PCV = conjugate, PPSV = polysaccharide)
    • Meningococcal (Neisseria meningitidis)
    • Haemophilus influenzae type B (Hib)
  3. Protein Subunit Vaccines
    • Pertussis (Bordetella pertussis) (aP in DTaP/Tdap)

@usmlereviews

174
Q

which one is good
vaccine or AB >?

A

๐Ÿ’‰ vs. ๐Ÿฆ  Vaccine vs. Antibody Therapy

๐Ÿ”น Vaccine (Active Immunity) โœ… Best for Prevention
- MOA: Stimulates immune memory (B/T cells).
- Duration: Long-term (years-lifetime).
- Types: Live, inactivated, subunit, toxoid.
- Example: MMR, DTaP, Hep B.

๐Ÿ”น Antibody Therapy (Passive Immunity) โœ… Best for Immediate Protection
- MOA: Pre-formed IgG Abs neutralize pathogen.
- Duration: Short-term (weeks-months).
- Types: Monoclonal Abs, IVIG, convalescent plasma.
- Example: RhoGAM, Tetanus Ig, Rabies Ig.

Best Choice?
- Prevention โŸถ Vaccine.
- Immediate protection (high-risk exposure, immunocomp.) โŸถ Antibody.

@usmlereviews

175
Q

Which AB not like AB ?

176
Q

IGd koi <

177
Q

CMI kivabe hoy ?

178
Q

HI kivabe hoy >

179
Q

autoimmunity ki mediated ?

A

cell
B & T cell

180
Q

which pathway first and why ?

A

๐Ÿ›ก๏ธ Complement Activation: First Pathway?

๐Ÿ”น Alternative Pathway (First) โœ… Always Active
- MOA: Spontaneous C3 hydrolysis (tickover).
- Why? No need for Abs, innate defense.
- Fastest response to pathogens (LPS, fungi, bacteria).

๐Ÿ”น Lectin & Classical (Delayed)
- Lectin: MBL binds mannose (bacterial sugars).
- Classical: C1 binds IgG/IgM (adaptive, needs Abs).

@usmlereviews

181
Q

role of 8 ?

A

MHC-II = 4
MHC-I = 8

182
Q

How APC cell present atg ?

A

APC must have MHC-I / II
present to T cell (CD 4/8)

342

APC - Co-stimulation

183
Q

MHC ki RBC te pawa jay >

A

immature e
cause tara neucleated

184
Q

toxin er against e kon complement ? a

A

alternative

185
Q

IgM IgG er agaiant kon complement ?

186
Q

smallest AB ?

187
Q

largest AB >

188
Q

no MHC where in body ?

A

Both MHC-I & II Absent โŒ

Corneal Cells (Immune privilege โ›” rejection).
Sperm Cells (partially) (Immune tolerance).
189
Q

atg-ab reaction name inside and outside the body ?

A

๐Ÿฆ ๐Ÿ”ฌ Ag-Ab Reaction (In Vivo vs. In Vitro)

๐Ÿ”น Inside Body (In Vivo) ๐Ÿฅ
- Neutralization (Toxins, viruses blocked).
- Opsonization (IgG tags for phagocytosis).
- ADCC (Antibody-Dependent Cell-Mediated Cytotoxicity) (NK cells kill).
- Complement Activation (Classical pathway โฌ† C1 binding).
- Immune Complex Formation (Type III hypersensitivity).

๐Ÿ”น Outside Body (In Vitro) ๐Ÿงช
- Precipitation (Soluble Ag + Ab โ†’ visible complex).
- Agglutination (Particulate Ag + Ab โ†’ clumping, e.g., ABO test).
- ELISA (Ag-Ab binding โ†’ color change).
- Western Blot (Protein-Ab detection).
- Immunofluorescence (Tagged Abs detect Ag).

@usmlereviews

190
Q

APC in which type of immunity ?

A

Adaptive immune response

191
Q

are APC neucleated cell ?

192
Q

memory T cell which type of response ?

193
Q

how memory T cell produce >

194
Q

if antigen enter into the body how cell will determine whether CMI / HI needed ?

A

atg - outside the body โ€“ HI - AB
atg - inside the body CMI - cytotoxic T cell

195
Q

central tolerance kader beeshuu ?

196
Q

IL-4,5 from where in B cell ?

197
Q

IL4 ??

A

b CELL growth

198
Q

IL-5 ??

A

B cell differentiation

199
Q

why Type=4 delayed ?

A

starts hours/days after contact with the ATG
last for days

200
Q

which cell in type-4 ?

A

helper + cytotoxc
389

201
Q

epitope spreading disease /

A

SLE
chrons disease
ulcerative collitis
IBD

202
Q

coxsackie disease ?

A

myopcarditis
DM-1

203
Q

sensitive test for SLE ?

A

Anti-nuclear antibody
ANA test

204
Q

type 5 hypersensitivity?

A

graves d
myasthenia gravis

205
Q

type 5 what ?

A

AB target surface receptor that are activated by hormones

206
Q

cell mediated killing // AB ?

Microbiology -Medical-Prof (49 decks)

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