Allergy was originally defined in 1906 in 1906 by Clemens von Pirquet as 'altered reactivity' to denote the different reaction which on second exposure to and antigen due to the formation fo antibodies, when compared to the first exposure. The term atopy decribes the clinical presentation of Type I hypersensitivity, which include asthna, eczema, hay fever and urticaria, These usually occur in subjects with a family history of these or similar conditions. The mechanism of allergy is the Type I hypersensitity reaction. contact with allergen results in its being processed by an antigen presenting cell and presented to T helper cells which then help B cells to IgE antibody. The IgE antibody is rapidly taken up via its Fc portion by mast cells and basophils, which are then senitized. Subsequent contact with same allergen will result in the cross-linking of IgE molecules by their fab portions which cause cell degranulation and mediator release. The contribution of genentic factors to the development of atopy has been an intriguing issue. The exact controlling mechanisms of the genetic factors are unknown, but there are many studies support the genetic controls of the development of atopy. Abnormally high levels of IgE synthesis and associated atopy often run in families. Althouth the full inhritance pattern is probably multigenic, family studies has shown that their is clear autosomal transmission of atopy. The ability to make specific IgE antibodies to certain antigens, e.g., ragweed pollen, is also inherited and may be linked to particular class II major histocompatibility complex alleles. Therefore, I think that the clinicians must consider the environmental and genetic factors when evaluate the atopic disease.
Alleles ; Ambrosia ; Antibodies ; B-Lymphocytes ; Basophils ; Cell Degranulation ; Eczema ; Genetics* ; Humans ; Hypersensitivity* ; Hypersensitivity, Immediate ; Immunoglobulin E ; Major Histocompatibility Complex ; Mast Cells ; Pollen ; Rhinitis, Allergic, Seasonal ; T-Lymphocytes, Helper-Inducer ; Urticaria

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Interstitial lung disease is a generic term for a heterogeneous group of lung disease that primarily affect the interstitium although the disease is not clearly restricted to the interstitium. The majority of interstitial lung diseases represent inflammatory insults to the microscopic anatomic space bounded by the basement membrane of epithelial and endothelial cells, which may occur as slowly developing process and ultimately end up as end-stage honeycomb fibrosis. The currently prevalent classification of interstitial pneumonia with practical utility and easy reproducibility pertaining only to idopathic interstitial pneumonia encompasses several different entities some of which may represent different aspects of the same condition. Honeycomb fibrosis is usually caused by a variety of pulmonary disease including chronic interstitial lung disease. It is important to recognize that usual inter-stitial pneumonia and honeycomb fibrosis are not synonymous. In the era of chemotherapy for malignant tumor, aggressive immunosuppression for autoimmune diseases and transplant recipients and acquired immunodeficiency syndrome, lung disease in the immunocompromised host has been common. Diagnostic lung biopsy becomes increasingly needed because proper treatment of interstitial lung disease relies on correct morphologic diagnosis. This review summarizes the pathologic spectrum of idiopathic interstitial pneumonias together with other inflammatory process with known or suggestive etiologies simulating interstitial pneumonias.
Acquired Immunodeficiency Syndrome ; Autoimmune Diseases ; Basement Membrane ; Biopsy ; Classification ; Diagnosis ; Drug Therapy ; Endothelial Cells ; Fibrosis ; Idiopathic Interstitial Pneumonias ; Immunocompromised Host ; Immunosuppression ; Lung ; Lung Diseases ; Lung Diseases, Interstitial* ; Pathology* ; Pneumonia ; Transplantation

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Family Characteristics* ; Hepatitis B Surface Antigens* ; Hepatitis* ; Humans

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Asthma* ; Epidemiologic Studies*

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Vibrio vulnificus* ; Vibrio*