مقدمه ای بر ایمنی شناسی

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بسم الله الرحمن الرحیم 

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a (۳۹ 1 سه شنبه 20/11/94 مقدمه و خصوصیات عمومی پاسخ های ایمنی دکتر گرگین 2 یک شنبه 25/11/94 سلول ها ى سيستم يمني دکتر سالاری 3 سه شنبه 27/1۱/94 ارگان های سیستم آیمنی 4 یکشنبه 2/12/94 گردش و لاله گزینی لنفوسیت ها دکتر سالاری 5 سه شنبه 4112/94 ‎cool‏ ذاته, و اجزاء آن دکتر سالادی 6 یکشنبه 9/12/94 آنتی ژن و ایمونوژن 7 اسه شنيه 11/12/94 آنتی بادی و *1621: ساختمان. انواع کلاس ها و مشخصات دکتر گرگین 8 یکشنبه 16/12/94 نت , بادی و کاربردهای ‎oi‏ دکر دنس 9 سه شنبه 18/12/94 این ها و نقش آنها در سیستم ایمنی دكت سالاری 10 سه شنبه 25/12/94 آنتی ژنهای اصلی ساز گاری بافتی ((1۳10 1 یکشنبه 15/1/95 سا وکارهای سلولی و مولکولی پردازش و عرضه آنتی ژن دکتر تقدسی 12 سه شنبه 1711/95 ژنتيك آنتی بادی و ‎TCR‏ دکتر سالاری 13 يكشتبه 22/1/95 مراحل تکامل و بلوغ لنفوسیتهای ظ و ۲" دکتر سالاری 14 سه شنبه 2411/95 نحوه فعال سازی لنفوسیت های 1 در پاسخ به آنتی ژن 15 يكشنبه 29/1/95 ك3 على ليا امد لول ‎iia‏ دكت كيد 

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do 17 18 19 20 21 22 23 24 متابع: اسه شنيه 900/99 یکشنبه 65/9/9 سه شنبه 2/9/95" یکشنبه 48/9/99 سه شنبه ا كشب ووره49/9 سه شنبه 90/9/99 66/۵۳ اسه شنبه 60/۳ سه شنبه نحوه فعال سازي و پاسخ لنفوسیت هاي 8 به آنتي ژن مکانیسم هاي اجرايي ايمني هومورال و کمپلمان ايمني مخاطي و نواحي معاف از سیستم ايمني ایمنوتولرانس (تحمل ایمنی) مکانیسمهای دفاع میزبان در برابر انواع میکروبهاء واکسن و واکسیناسیون ايمنولوژي تومور ايمنولوژي پیوند ایمنوهماتولوژي حساسیت شدید نوع | (آلرژي) دکتر سالار دکتر سالار: دكار سره دکتر نقدسی دکتر سالار: دکتر گرگین دکتر تقدسی دکتر گرگین دکتر گرگین 1- Cellular & molecular Immunology, by: Abul K. Abbas and A. H. Lichman (8" edition 2015) 2- Medical Immunology, by: D. Stites et al. (last edition) 

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سنجش و ارزیابی آزمون کوئیز أزمون ميان ترم آزمون پایان ترم سور فل در كلاس روش تستی و تشریحی پرسش و پاسخ سهم از نمره كل (بر حسب درصد) ۵ نمره 06 نمره 06 نمره 6 نمره مقررات كلاس و انتظارات از دانشجو: 1- حضور منظم و بدون غيبت در كلاس 2- انتظار حضور سر وقت دانشجو در كلاس تاريخ هه ند شنبه 0 ©/0/ 66 3- انتظار مطالعه یا نگاه مروری بر مطلب ارائه شده در هر جلسه قبل از كلاسن شروع جلسه 12.30 

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‘immunology Gay tracert Relies tty ۱ 

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* اصطلاح 112212211131177 از وازه 111213211131125 به معنى ‎own reer) pee pomp ye Creer cre were] Cos) Relea Way er)‏ ee BOS eB es cece Dc nee Tod ‏حاصل مي شود, اساس شكل كيري وازه ايمني است.‎ ا ال ات ل لت 0 ۳ مختلف 0-6 داشته است. اما ‎eo‏ مدارک مستند ‎iTS) eee)‏ 7 Pewee Beene F erenpeg eee Bere rn ‏بهبود ۳۹۳ ۳ ابله‎ ۳ oer) ‏پوستولهاي پوستي‎ ‏افراد استفاده مي شده و‎ rower) ‏مصون‎ 2000 در تركيه از تلقيح انها. 

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و ‎ey‏ ل ‎ee‏ ‏گرفت (1798). [| ۲ | پوستي افراد مبتلا به آبله گاوي را با خراش ‎ee renee Ce neers Some sce re erne epee‏ مبتلا به آبله انسانى را به او منتقل كرد و مشاهده كرد كه يسربجه سألم 9 ۱ ‎eee‏ از کشت کهنه عامل وباي جوجه. واکسن ساخت و بدنبال آن بر علیه سیاه زخم گوسنند و هاري واکسن ساخت. ‏ل ‎Sore me TS‏ و ور رس ‎Leer nT]‏ 0 050 

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Edward Jenner (1749-1823) 

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Koch’s Postulates Metchnikoff Phagocytosis Miller Jenner 5 ۳ Miller Kohler & Milstein Monoclonal Abs Jansen Microscope Bacteria Vaccination Antisera 7 Cells 

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- Von Behring (1854~1917) discovered the antitoxin and the principles of antiserum therapy. He established one of the first corporations to product 12 immunologic — > products.27. —— 

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Clonal selection theory and immune tolerance The Nobel Prize in Physiology or Medicine 1960 "for discovery of acquired immunological tolerance" Sir Frank Macfarlane Peter Brian Medawar ۴ 

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Lymphocyte ‏بسح‎ precursor, Mature Lymphocyte © lymphocyte clones mature in generative go ff. SON lymphoid organs, in the absence of antigens Clones of mature lymphocytes specific for diverse antigens enter lymphoid tissues | Antigen X Antigen-specific clones are activated ("selected") by antigens Antigen-specific immune responses occur <a 

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MHC The Nobel Prize in Physiology or Medicine 1980 “for their discoveries concerning genetically determined structures on the cell surface that regulate immunological reactions" وک حر Baruj Benacerraf Jean Dausset George D. Snell 

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Monoclonal Antibody Niels K. Jerne Georges J.F. Kohler César Milstein The Nobel Prize in Physiology or Medicine 1984 was awarded jointly to NielsK. ۴ Jeme, Georges J.F. Kohler and César Milstein "for theories concerning the ‏عه‎ ‎‘Specificity in development and control of the immune system and the discovery of ‏سب‎ ‎principle for production of monoclonal antibodies". 

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Antibody Diversity Susumu Tonegawa is a Japanese Scientist who won the Nobel Prize for physiology or medicine in 1987 "for his discovery of the genetic principle for generation of antibody diversity" 

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Peter C. Doherty Rolf M. Zinkernagel Winner of ‏لت‎ 6 obel Prize in Physiology or Medicine for discovery of how the immune system rec virus-infected cells ‏و‎ BS. 

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BRUCE A. BEUTLER The Nobel Prize in Physiology or Medicine 2011 was divided, one half jointly to Bruce A. Beutler and Jules A. Hoffmann 'for their discoveries concerning the activation of innate immunity" and the other half to Ralph M. Steinman ‘for his discovery of the dendritic cell and its role in adaptive immunity". 

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11111111111 0 ° Immune system: The cells and molecules responsible for immunity. ¢ Immune response: Collective and coordinated response of Immune system to foreign substances. ° The physiological function of the immune system is defense against infectious microbes & microbial products & also tumors. 

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۰ ]101۳0102۳۵۵ ۲66۵01۴۵66۵: ‏عطا ۵۶ جمناممع1 ه و1‎ Immune system to components of microbes as well as to macromolecules, such as proteins and polysaccharides, and small chemicals that are recognized as foreign. Immunology: is the study of immune responses in this broader sense and of the cellular and molecular events that occur after an organism encounters microbes and other foreign macromolecules. 

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Types of IMMUNITY * Immunity against microbes is mediated by: 1.Innate (natural) immunity: ¢ Early, rapid responses, but limited & non-specific. 2. Adaptive (acquired) immunity: ٠ Take time but powerful , specific & have ۱۹۹۵ * Induced by Lymphocytes (B & T cells) ., 

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Microbe Innate immunity Adaptive immunity ‎Epithelial‏ لا ‎barriers ‎B lymphocytes Antibodies ‎1 ‎Phagocytes Dendritic cells ‎Complement NK cells, omplement ‏مک‎ ‎Hours ‎0 6 12 ١ Time after infection > ‎FIGURE 1-1 Innate and adaptive immunity. The mechanisms of innate immunity provide the initial ‎ 

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Adaptive For microbial and non- microbial antigens Very large; receptors are produced by so- matic recombination of gene segments Yes Yes Lymphocytes in epithelia; antibodies secreted at epithelial surfaces Antibodies Lymphocytes TABLE 1-2 Features of Innate and Adaptive Immunity Innate For molecules shared by groups of related microbes and mol- ecules produced by damaged host cells Limited; germline encoded None Yes Skin, mucosal epithelia; antimicrobial mol- ecules Complement, othors. Phagocytes (macro- phages, neutrophils), natural killer calls, innate lymphoid cells Characteristics Specificity Diversity Memory Nonreactvity toself Components Cellular and chemical barriers Blood proteins Cells 

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Innate immunity ¢ Innate immunity (natural or native immunity): provides the early line of defense against microbes -It consists of cellular and biochemical defense mechanisms that are in place even before infection and respond rapidly to infections. - These mechanisms react to microbes & their products & injured cells, and they respond in essentially the same way to repeated ۱۹۹ ‏جو‎ 

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Components of innate (0) . Physical and Chemical barriers: Skin and Mucosal Epithelia and anti-microbial chemicals produced at epithelial surfaces. . Phagocytic cells (Neutrophils, Macrophages), Dendritic cells, & Natural killer (NK) cells. . Blood proteins: members of the complement system and other mediators of inflammation. . Cytokines: Proteins that regulate and coordinate many of the activities of the cells of innate & adaptive immunity. 

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INNATE IMMUNITY Barriers 1- Anatomic (physical) Chemical barriers: A. Skin 0 Epidermis: Epithelial cell layers and antimicrobial chemicals (fatty acids & acidic PH and microbial normal flora). 0 Dermis: Dipper layer of skin which contain blood vessels, nerves, sweet glands and hair follicles. 

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ملحن ۱ 70 خفن | ها سا Nerve and VasculirSupply ‏متا فص ممصيف؟‎ ii Muscle 

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B. Mucosal membrane: ‏عدع:123 لمتاع طاغأزمع ه‎ o Mucus & Beating cilia, o Tears, saliva, urine, stomach acid. ۱ 0 Lysozyme 2- Phagocytic cells (Macropisay Neutrophile), Dendritic cells, NK cells, Mast cells, basophiles & Eosinophiles, Platelets. 

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3- Blood proteins * Complement System: Plasma & membrane proteins that when activated can induce inflammation, lysis bacteria , facilitate phagocytosis. * Kinin system, Fibrinolitic system, ° Inflammation: is a defense mechanisms in which blood cells and proteins migrate to the site of infection to combat microbes. - Inflammation sign: Redness, Swelling, Heat & Pain 

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‎firm adhesion transmigration‏ 0 0 ره ‎0 ‎ ‎ ‎neutrophil ‎- Tio Ho 6 @ ‎Ant‏ | بیع ‎so‏ ‎endathelium ‎tissue ‎ ‎chemotaxis‏ جد ‎os to site of infection‏ ‎ 

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4- Cytokines: - Hormone like proteins which produce by leukocytes & other cells and affect Immune cells. -Include: Interleukins (IL-1 to IL- 35), Interferon (IFN-a, IFN-B & IFN-y), Tumor necrosis factor (TNF), ...... 

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Adaptive immunity ¢ Adaptive Immunity: stimulated by exposure to microbes and with re-exposure make a faster and more powerful responses. * Because this form of immunity develops as a response to infection and adapts to the infection, it is called adaptive immunity. ¢ It has a huge capacity to distinguish between different microbes and molecules, and for this reason it is also called Specific immunity 

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Types of Adaptive Immuny ° There are two types of adaptive immune: 1. Humoral immunity is mediated by molecules in the blood and mucosal secretions, called antibodies, which are produced by B lymphocytes. 2. Cell-mediated immunity, also called cellular immunity, is mediated by T lymphocytes. 

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FIGURE 12 Types of adaptive ‏سس سس سس‎ iumoral Call-mediated immunity. In humoral immunity, 8 ran. Tay lymphocytes secrete antbodies that preventinfectionsendeliminate extacellular microbes. In cell-mediated immunity, heber T lymphocytes activate macrophages to | Microbe 05 x x kill hagacytesed microbes, or cy:otoxi: T ۱ Invaceluar Iymphoojts drecty destroy nfectod cel. a Extracellular Phagocytcsed | microbes microbes | macrophage ating within | pected cot Responding ‏اب تسا شا‎ 0 ie 0 ‏ات‎ Tiymphocyte | T ‏با‎ ‎١ ‎Secreted ' anthody ! Effector ve ۱ mechanism ' Sorum ۱ 0 Cannes Block Activate infections and}|| macrophages Functions eliminate to kill extracellular | || phagocytosed| microbes cells and eliminate reservoirs of infection | 

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TABLE'-3 Cardinal Features of Adaptive Immune atte una rasponse microbe (x aanmiroil angen) targeted to that microbe fr antigen) les the immune sytem to respond argo varity of ation ineroases tho aby to cambat peat infections by the sama microbe increases the number of angen speci phocytes ates esposes tat are optimal tor dotonso gains citron yp صا ‎eters‏ م ‎tin‏ سال | ‎spond to new encountered an‏ Proven juny tothe host rng Responses Feature ‏ا‎ peasy Diversity Mamory ona expansion Nonreactvy si 

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۱ * ايمنى اكتسابى آنتى رنها و در اصل بخش هاى مختلف يك آنتى ‎CS)‏ م ا ل 0 أنتى زن را بوسيله يك رسيتور اختصاصى شناسايى مى كند. ا دو كذ( ا ل ا ل لل شناسایی کند. برای هر یک از این آنتی ژنها یک لنفوسیت اختصاصی وجود دارد که آنتی ژن را از طریق رسپتور اختصاصی شناسایی می کند. لذا لنفوسیت ها متنوع هستند. 

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خاطره -122631321017973 601621 ۱ ليمني ۱ عليه ياتوزنى كه قبلا با ان برخورد داشته است را خاطره ايمنى كويند. ‎Secondary exposure to specific‏ - ‎antigen elicits a stronger & faster‏ ‎immune reaction‏ 

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Clonal ۱۱۱۱ ‎aed a‏ ب ۱۳ ‎kes)‏ ل ل برخورد با آن آنتی ژن فعال شده و تکثیر پیدا مي کنند و كلون هاى سلولي را بوجود مي آورند. ‏* سلولهابي كه از تكثير يك سلول حاصل مي شوند, را يك كلون سلولی نامند. ‎Specialization -5 ‏7 سيستم ايمنى برای افزایش خاصیت ضد میکروبی. در مقابل ل لل ا ا 30 باكتريهاى خارج سلولى ياسخ هومورال و در مقابل باكترى هاى داخل سلولى ياسخ سلولى مى دهد. 

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| Se ke ees erence a Peder rede nits BE ES cet eee ned labia = Non-reactivity to self -7 0 te ere we ‏ا‎ همين دليل در حاليكه به آنتى زنهاى بيكانه باسخ مى دهد . ۱ 

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‎B cell +0۳ B cell‏ سل ‎ ‎ ‎ ‎ ‎ ‎Piasma cells Antigen X x Antigen X + Antigen Y 0 | | ek ۲ x Plasma call 9 ‘Secondai ۲ ‏در‎ ۷ Ys response ‏اجر مس‎ 90 / 3 Memor | Prima \ @ y +0 caer < Primary kam B cells response / ۵00-۷ ” 5 ‏ا‎ ‎5 a == ‏سچست‎ ras se 5 = oa 7 35 ۳ x 2 4 6 8 10 ‎Weeks ‎1-4 Specificity, memory, and contraction of adaptive Immune responses. ‏ت‎ 

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Cellular Components of the Adaptive Immune System ا لف الاك ار ‎system are:‏ ‎-Lymphocytes: B cells, T cells (T‏ ‎helper, T cytotoxic & T regulator).‏ - Antigen presenting cells (APC): Dendritic cells. -Effector cells: Macrophages & other cells. 

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Antigen recognition Effector functions phagocytosis, ‘complement Activation of macrophages Inflammation [| presented sored | ‘Activation By antigr (proliferation and differentiation) resenting colt of TandB lymphocytes Infected call expressing microbial antigen 1 تسم ‎ry + > -# footed cell‏ ديه “Regulatory ==, 6. 

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Type of Adaptive Immunity based تت افمط ‎Foreign origin‏ icrobial ch infection 

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11 ) 112112111111 52661162 01 دعم 1- Active: Se NC Lana VIN ‏ان ال ا‎ - Artificially: Vaccination 2- Passive: - Naturally: Placental transfer of antibody - Artificially: Administration of antitoxin 

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Overview of Immune Responses to Microbes ا رت ۱۱۱۱۱۱۱۱۱۱ ۱۱۱۱۱۱ :۱۱:۱ | 1۱۷10۳۵۵۵ - Inflammation - Anti-viral defense: Production of Interferon which make cells resistant to viral infection and killing of virus-infected cells by NK cells. ¢ The Adaptive Immune Response: - Secreted antibodies - Cytotoxic T lymphocytes (CTLs) -T helper & Phagocytes 

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‘Antigen Lymphocyte Antigen Contraction recognition activation elimination _(homeostasis) Effector T Antibody ‏خر‎ ‎producing & 'ympnocyie Memory هناش ‎and effector‏ Tcells Surviving memory calls Antigen presenting * Naive T ۹۹ lymphocyte Naive B lymphocyte 7 Days after antigen exposure FIGURE 1-6 Phases of adaptive immune responses. ‏اث‎ 

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