KEY ELEMENTS OF ALLERGIC DISEASES [アレルギー]
KEY ELEMENTS OF ALLERGIC DISEASES
ALLERGENS. The term allergen refers to an antigen that triggers an IgE response in genetically predisposed individuals. Most allergens are proteins that have molecular weights of 10-70 kDa; molecules <I0 kDa do not bridge adjacent IgE antibody molecules on the surface of mast cells or basophils; most molecules >70 kDa do not pass through mucosal surfaces needed to reach
antigen-presenting cells for stimulation of the immune system. Allergens frequently function in their natural state as proteolytic enzymes, which may contribute to increased mucosal permeability
and sensitization. This includes a number of major allergens such as Dermatophagoides pteronyssinus allergen I (Der p 1) from the house dust mite.
T CELLS. All individuals are exposed to potential allergens. Nonatopic subjects respond with the proliferation of T helper type 1 (Th1) cells, which secrete cytokines, including interferon (IFN)-gamma, that are involved in the elicitation of allergen-specific IgG antibodies. Th1 cells are typically involved in the eradication of intracellular organisms such as mycobacteria, because of the ability of Th1 cytokines to activate phagocytes and promote the production of opsonizing and complement-fixing antibodies. Genetically predisposed atopic individuals respond with a brisk expansion of T helper type 2 (Th2) cells that secrete cytokines favoring IgE synthesis and eosinoohilia.
Atopic responses include the generation of allergen-specific IgE antibodies that are detectable by serum testing or positive immediate reactions to allergen extracts on prick skin testing (see Chapter 140). The Th2 cytokines interleukin (1L)-4 and IL-13 play a key role in immunoglobulin isotype switching to IgE (Fig.139-1). IL-5 and IL-9 further enhance IgE synthesis and play an important role in the differentiation and development of eosinophils. The combination of IL-3, IL-4, and IL-9 contributes to mast cell development. Th2 cytokines play an important role in the pathogenesis of asthma and allergic diseases; Th2 cells infiltrate into the affected tissues of acute allergic tissue reactions. Chronic allergic reactions often are characterized by the infiltration of Th1 and Th2 cells. This is important because Th1-type cytokines such as IFN-gamma can potentiate the function of allergic inflammatory effector cells such as eosinophils and thereby contribute to disease severity.
A small subset of T cells referred to as T regulatory (Treg) cells are thought to play a critical role in allergic and autoimmune diseases. These cells have the ability to suppress effector T cells of either the Th1 or Th2 phenotypes involved in mediating inflammation in a direct cell-contact or antigen-specific manner. Treg cells express CD4+CD25+ surface molecules and immunosuppressive cytokines such as IL-10 and transforming growth factor (TGF)-beta1. The forkhead/winged-helix transcription factor gene FOXP3 is specifically expressed by CD4+CD25+ Treg cells and programs their development and function. Adoptive transfer of Treg cells inhibits the development of airway eosinophilia and protects against airway hyperreactivity in animal models of asthma. Patients with mutations in the human FOXP3 gene lack CD4+CD25+ Treg cells and develop severe immune dysregulation with polyendocrinopathy and food allergy and high serum IgE levels (XLAAD/IPEX disease) (see Chapter 125). It is thought that CD4+CD25+ Treg cells play an important role in controlling the allergic immune response and the lack of such cells may predispose to the development of allergic diseases.
ANTIGEN-PRESENTING CELLS (APC). Dendritic cells, Langerhans cells, monocytes, and macrophages play an important role in the induction of allergic inflammation by presenting allergens to T cells and by contributing to the local recruitment of effector cells. APCs are a heterogeneous group of cells with the common property of presenting antigens in the context of the major histocompatibility complex (MHC). Dendritic cells and Langerhans cells are unique in their ability to prime nai've T cells and are responsible for the primary immune response, which is the sensitization phase of allergy. APCs are found primarily in lymphoid organs and the skin. Monocytes and macrophages likely play more of a role in activating memory T-cell responses, which occurs during the elicitation phase of allergy.
Dendritic cells residing in peripheral sites such as the skin, intestinal lamina propria, and lung are relatively immature. These immature dendritic cells take up antigens in tissues and then migrate to the T-cell areas in locally draining lymph nodes. During this migration, they undergo phenotypic and functional changes characterized by increased expression of MHC class I, MHC class II, and co-stimulatory molecules that react with CD28 expressed on T cells. In the lymph nodes, they directly present processed antigens to resting T cells to induce their proliferation and differentiation.
Based on their ability to favor Th1 or Th2 differentiation, mature dendritic cells have been designated as DC1 or DC2, respectively. The critical factor for the polarizing mechanism to Th1 cells is the level of IL-12 produced by DC1 cells. Differentiation of T cells in the absence of IL-12 production by DC2 leads to Th2 cells. Histamine and PGEz inhibit IL-12 production and contribute to the development of DC2. A unique feature of atopy is the presence of allergen-specific IgE on the cell surface of their APCs. Importantly, the formation of Fc E receptor I (FcERI)/IgE/allergen complexes on the APC cell surface markedly facilitates allergen uptake and allergen presentation. The clinical importance of this phenomenon is supported by the observation that FceRI-positive Langerhans cells bearing IgE molecules is a prerequisite for provocation of eczematous lesions by aeroallergens applied to the skin of patients with atopic dermatitis. The role of the low-affinity IgE receptor Fc E receptor II (FceRII, CD23) on monocyte-macrophages is less clear, although it
appears that under certain conditions it can also facilitate antigen capture. Cross linking of FcERII as well as FceRI on monocyte-macrophages leads to the release of inflammatory mediators.
飲食알레르기 VS 飲食過敏 [アレルギー]
food allery vs food intolerance
離乳食을 始作하는 아이들은 어떤 飲食을 먹으면 배탈이 나는 경우가 있다. 배에 가스가 차고 방구를 자꾸 끼고 보채고 嘔吐하고 泄瀉하기도 한다. 이런 境遇 흔히 飲食알레르기라는 말을 하기도 하지만, 진짜로 免疫体系가 作用하는 飲食알레르기는 거의 없고 大概의 境遇는 飲食過敏(food intolerance)인 것이다.
万一 아이들의 健康上 摂取하는 것이 必須的인 飲食이라면 좀 더 慎重하게 알레르기라는 말을 하는 것이 좋다. 어떤 飲食을 처음 始作해서 問題가 있었더라도 時間이 지나서 아가의 腸이 튼튼해지면 問題가 없어지는 境遇가 많기 때문에 나중에 다시 먹이는 것이 좋다. 普通은 1-3個月 間隔을 두고 다시 始作. 이때에도 아가가 飲食을 먹고 배탈이 나면 다시 몇個月 그 飲食을 먹이지 말고 몇個月 後에 다시 먹여보는 것이 좋다.
飲食 때문에 생기는 問題는 主로 돌 以前에 생기며 3살이 지나면서 顕著하게 減少한다. 돌이 지나면 아가의 腸이 어느 程度 튼튼해져 前에 問題가 있었던 飲食의 大部分을 먹을 수 있다. 特히 돌 以前에는 鶏卵 흰자나 밀가루 生牛乳나 오렌지나 감귤같은 飲食은 아이가 먹고 탈나는 境遇가 많기 때문에 避할 수 있으면 避하는 것이 좋다.
food allergy 와 food intolerance는 다른 問題다. food allergy는 免疫体系가 作用해서 생기는 問題이지만 food intolerance는 免疫体系와는 相関없이 먹는 飲食에 敏感해서 생기는 問題로 adverse reactions to foods라고 말하기도 한다.
food allergy Sx : 알레르기의 特徴的인 症状들이 나타나게 된다. 눈물, 콧물, 가려워 눈을 비비기, 눈周囲, 입, 입술, 입안, 목구멍의 浮腫으로 목소리가 쉬고 숨이 막히기도. 嘔吐, 泄瀉, 甚하면 血便. 몸에 発疹이 돋거나 두드러기가 생기기도. 기침, 재채기, 呼吸困難, 喘鳴音. 熱은 普通(-)
3歳 以前에 food allergy가 생긴 아이들은 大概 7歳 以前에 좋아지며 3歳 以後에 food allergy가 생긴 아이들은 잘 克服하지 못할 可能性이 높다. 牛乳알레르기가 있는 아이들은 3歳까지는 95%가 好転된다. 하지만 땅콩이나 조개種類는 알레르기가 平生을 持続하는 수가 많다.
美国小児科学会에서 아가가 알레르기가 걸릴 可能性이 높은 집안에서 태어난 境遇 다음의 몇가지를 注意하기를 勧奨한다.
1. 엄마가 妊娠中에 特別히 飲食을 가릴 必要는 없다.
2. 可能하면 6個月까지는 母乳를 먹이고 粉乳를 먹일 때는 알레르기 粉乳를 먹이는 것을 勧奨. 代表的인 것이 HA粉乳. 豆乳나 콩으로 만든 粉乳같은 것은 勧奨하지 않는다.
3. 母乳授乳 엄마는 堅果類나 땅콩같은 것은 避하고 鶏卵과 牛乳도 避하는 것이 좋다.
4. 離乳食은 4-6個月이 되거든 始作하는 것이 좋다.
5. 生牛乳는 1歳부터, 鶏卵은 2歳부터, 生鮮은 2-3歳, 땅콩과 堅果類는 3歳가 되거든 먹이기 始作. 堅果類를 그대로 먹이는 것은 滿 4歳는 지나야 한다.
하지만 生鮮의 境遇 우리나라에서는 普通 돌이 지나면 먹이는 境遇가 많으며 大概의 境遇 큰 問題가 없다.
<参考>
河正勳小児科
알레르기患者 生活習慣改善 [アレルギー]
* 愛玩動物 키우지 않는다.
* 메밀베개, 털이 북실북실한 人形을 없앤다.
* 淸掃를 徹底히 한다.
* 化粧品은 可及的 使用을 줄인다.
* 吸煙禁止.
* 가스렌지 후드를 꼭 使用한다.
<参考>
河正勳小児科
