Hla in Cryptogenic Fibrosing Alveolitis

Turton, Charles; Morris, Lauren; Lawler, SylviaD.; Warwick, Margaret

doi:10.1016/s0140-6736(78)90178-2

Cited by 38 publications

(18 citation statements)

References 5 publications

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“…The association between pulmonary fibrosis and HLA genes has been examined in several studies. Association with the HLA class I genes B7, B8 and B12 and the HLA class II gene DR2 was inconsistently found and not confirmed by published studies [118][119][120][121].…”

Section: Pulmonary Fibrosismentioning

confidence: 76%

Immunogenetic basis of environmental lung disease: lessons from the berylliosis model

Saltini¹,

Amicosante²,

Franchi³

et al. 1998

Eur Respir J

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The role of genetic factors has been hypothesized in the pathogenesis of a number of chronic inflammatory lung diseases. The genes of the major histocompatibility complex (MHC) locus on human chromosome 6 have been identified as important determinants in diseases caused both by inorganic and organic compounds such as beryllium, gold, acid anhydrides, isocyanates and grass pollens. Since many environmental factors are the determinants of the immunopathogenesis of asthma, pulmonary granulomatous disorders, hypersensitivity pneumonitis and fibrotic lung disorders, an understanding of the interaction between environmental factors is crucial to epidemiology, prevention and treatment of these disorders. Berylliosis is an environmental chronic inflammatory disorder of the lung caused by inhalation of beryllium dusts. A human leukocyte antigen class II marker (HLA-DP Glu69) has been found to be strongly associated with the disease. In in vitro studies, the gene has been shown to play a direct role in the immunopathogenesis of the disease. In human studies, the gene has been shown to confer increased susceptibility to beryllium in exposed workers, thus suggesting that HLA gene markers may be used as epidemiological probes to identify population groups at higher risk of environmental lung diseases, to identify environmental levels of lung immunotoxicants that would be safe for the entire population and to prevent disease risk associated with occupation, manufactured products and the environment. Studies on the associations between human leukocyte antigens and chronic inflammatory lung disorders are reviewed in the context of the berylliosis model.

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Section: Pulmonary Fibrosismentioning

confidence: 76%

Immunogenetic basis of environmental lung disease: lessons from the berylliosis model

Saltini¹,

Amicosante²,

Franchi³

et al. 1998

Eur Respir J

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“…Because of the very strong LD within this haplotype, it is difficult to precisely identify the particular disease-associated HLA allele among them, or distinguish the contributions of these HLA from other interspersed immunoregulatory elements, in lieu of focused, high-resolution genomic studies [21,38,39]. Almost all previous HLA characterizations of IPF patients date from before the development of precise and definitive molecular methodologies that distinguish these alleles [40][41][42][43][44][45] (Table 4). Moreover, only two of these early serologic-based determinations examined even a very restricted repertoire of the many, sincediscovered, Class II alleles [44,45].…”

Section: Discussionmentioning

confidence: 99%

“…The numbers of subjects among those investigations were also usually quite small (Table 4), severely limiting their power to detect intergroup differences. Despite these potential limitations, however, several of those earlier investigations indicated HLA allele frequency perturbations may be present in IPF [40,[43][44][45], although this finding was not invariable [41,42]. In particular, one of these earlier studies indicated that DR2, a serologic correlate of HLA-DRB1*15 and, generally much less frequently, HLA-DRB1*16 gene products, appeared to be over-represented in IPF subjects (45), a finding which may be congruent with the current results.…”

Section: Discussionmentioning

confidence: 99%

The HLA Class II Allele DRB1*1501 Is Over-Represented In Patients With Idiopathic Pulmonary Fibrosis

Xue¹,

Gochuico²,

Feghali‐Bostwick³

et al. 2011

C32. Studies of Lung Fibrosis, Copd and Airway Remodeling

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Background: Idiopathic pulmonary fibrosis (IPF) is a progressive and medically refractory lung disease with a grim prognosis. Although the etiology of IPF remains perplexing, abnormal adaptive immune responses are evident in many afflicted patients. We hypothesized that perturbations of human leukocyte antigen (HLA) allele frequencies, which are often seen among patients with immunologic diseases, may also be present in IPF patients.

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“…Interestingly, however, patient 1 with the most severe lung disease showed expression of HLA B7, and this antigen has been implicated to play a role in cryptogenic fibrosing alveolitis. 19 This may have made her more susceptible to the antigens than her siblings. Whether the HLA-typing of the father results in protection against PBL remains unknown, because he probably experienced less antigen exposure than the children.…”

Section: Discussionmentioning

confidence: 99%

A Family With Extrinsic Allergic Alveolitis Caused by Wild City Pigeons: A Case Report

2000

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ABSTRACT. We describe a family in which the mother died of unresolved lung disease and whose 5 children, some of whom had previous signs of asthma, were subsequently affected by extrinsic allergic alveolitis caused by contact with wild city pigeon antigens. The children received systemic corticosteroids for 1 month and inhaled steroids for 24 months, while antigen exposure was reduced as much as feasible. This was followed by a quick clinical recovery and a slow normalization of chest radiographs and pulmonary function indices, especially of diffusion capacity, during a follow-up of 24 months.Because pigeon-breeder's lung caused by free-roaming city pigeons has not been previously described, it remains unclear whether this family developed the disease because of high antigen exposure or because of increased susceptibility. None of the supposedly high-risk human leukocyte antigen types were found in the children. Whether human leukocyte antigen B7 in 1 child played a role in the course of the illness remains speculative. It is unknown to what extent pigeon-breeder's lung caused by nondomestic birds remains undetected and misdiagnosed as difficult or steroid-resistant asthma. The question remains whether free-roaming city pigeons are indeed a public health risk. We suggest that atypical outdoor antigens be considered in all patients with nonresolving chest disease or therapy-resistant asthma. Pediatrics 2000;105(5). URL: http://www.pediatrics.org/ cgi/content/full/105/5/e62; birds, extrinsic allergic alveolitis, asthma, outcome, follow-up, human leukocyte antigen.ABBREVIATIONS. PBL, pigeon-breeder's lung; IgG, immunoglobulin G; FEV 1 , forced expiratory volume in 1 second; FVC, forced vital capacity; TLC, total lung capacity; RV, residual volume; D L co, diffusion capacity of the lung corrected for hemoglobin and alveolar volume; HLA, human leukocyte antigen.

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Hla in Cryptogenic Fibrosing Alveolitis

Cited by 38 publications

References 5 publications

Immunogenetic basis of environmental lung disease: lessons from the berylliosis model

Immunogenetic basis of environmental lung disease: lessons from the berylliosis model

The HLA Class II Allele DRB1*1501 Is Over-Represented In Patients With Idiopathic Pulmonary Fibrosis

A Family With Extrinsic Allergic Alveolitis Caused by Wild City Pigeons: A Case Report

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