scholarly journals Fetal cell microchimerism: a protective role in autoimmune thyroid diseases

2015 ◽  
Vol 173 (1) ◽  
pp. 111-118 ◽  
Author(s):  
Valentina Cirello ◽  
Roberta Rizzo ◽  
Milena Crippa ◽  
Irene Campi ◽  
Daria Bortolotti ◽  
...  
Keyword(s):  
Human Leukocyte ◽  
Protective Role ◽  
Systemic Autoimmune Disease ◽  
Fetal Cell ◽  
Autoimmune Thyroid Diseases ◽  
Autoimmune Thyroid ◽  
Leukocyte Antigen ◽  
Fetal Cells ◽  
Maternal Immune System ◽  
Polymorphic Pattern

ObjectiveThe physiological persistence of fetal cells in the circulation and tissue of a previously pregnant woman is called fetal cell microchimerism (FCM). It has been hypothesized to play a role in systemic autoimmune disease; however, only limited data are available regarding its role in autoimmune thyroid disease (AITD).DesignCirculating FCM was analyzed in a large series of previously pregnant women with Graves' disease (GD), Hashimoto's thyroiditis (HT), or no disease (healthy controls (HCs)). To exclude the possible bias related to placental factors, the polymorphic pattern of human leukocyte antigen-G (HLA-G) gene, which is known to be involved in the tolerance of fetal cells by the maternal immune system, was investigated.MethodsFCM was evaluated by PCR in the peripheral blood, and the Y chromosome was identified by fluorescencein situhybridization in some GD tissues.HLA-Gpolymorphism typing was assessed by real-time PCR.ResultsFCM was significantly more frequent in HC (63.6%) than in GD (33.3%) or HT (27.8%) women (P=0.0004 andP=0.001 respectively). A quantitative analysis confirmed that circulating male DNA was more abundant in HC than it was in GD or HT. Microchimeric cells were documented in vessels and in thyroid follicles. In neither GD/HT patients nor HC women was theHLA-Gtyping different between FCM-positive and FCM-negative cases.ConclusionThe higher prevalence of FCM in HC as compared to GD and HT patients suggests that it plays a possible protective role in autoimmune thyroid disorders. Placental factors have been excluded as determinants of the differences found. The vascular and tissue localization of microchimeric cells further highlights the ability of those cells to migrate to damaged tissues.

scholarly journals Human Leukocyte Antigen HLA in Korean patients with Autoimmune Thyroid Diseases

1986 ◽  
Vol 1 (2) ◽  
pp. 243-249 ◽  
Author(s):  
Kap Bum Huh ◽  
Hyun Chul Lee ◽  
Hyeon Man Kim ◽  
Hye Ree Lee ◽  
Chein Soo Hong ◽  
...  
Keyword(s):  
Human Leukocyte Antigen ◽  
Human Leukocyte ◽  
Thyroid Diseases ◽  
Autoimmune Thyroid Diseases ◽  
Autoimmune Thyroid ◽  
Leukocyte Antigen ◽  
Korean Patients

scholarly journals Frequency of alleles associated with celiac disease in patients with autoimmune thyroid disease

2021 ◽  
Vol 34 ◽  
Author(s):  
Clédia Silveira Flores da SILVA ◽  
Natalia Rodrigues CARDOZO ◽  
Raíssa ZANATTA ◽  
Augusto SCHNEIDER ◽  
Carlos Castilho de BARROS ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Gastrointestinal Symptoms ◽  
Human Leukocyte ◽  
Thyroid Diseases ◽  
Autoimmune Thyroid Diseases ◽  
Autoimmune Thyroid ◽  
Leukocyte Antigen ◽  
Polymerase Chain ◽  
Genetic Profiles

ABSTRACT Objective To determine the frequency of Human leukocyte antigen alleles and to verify the association of the presence of these alleles with symptoms and other diseases related to celiac disease in patients with autoimmune thyroid diseases. Methods A questionnaire on the symptoms and diseases associated with celiac disease was applied. Genomic deoxyribonucleic acid was extracted by collecting cells from the oral mucosa. The alleles (DQA1*0501; DQB1*0201; DRB1*04) were identified by means of the polymerase chain reaction. Results A total of 110 patients with autoimmune thyroid diseases participated in this study. It was observed that 66.4% of the individuals carried at least one of the alleles assessed and that 58.2% of the individuals were positive for at least one of the DQ2 alleles (DQA1*0501; DQB1*0201) and out of these 18.2% were positive for both DQ2 alleles (DQA1*0501; DQB1*0201). With regard to DQ8 (DRB1*04), 21.8% of the studied population was positive for this allele and 3.6% was positive for both DQ2 (DQA1*0501; DQB1*0201) and DQ8 (DRB1*04). A significant association was found between the presence of the DRB1*04 allele and gastrointestinal symptoms (p=0.02). A significant association of the DRB1*04 allele with type 1 diabetes mellitus (p=0.02) was observed. Conclusion The genetic profiles most commonly associated with celiac disease, such as DQ2 (DQA1*0501; DQB1*0201) and DQ8 (DRB1*04) were around 20.0% prevalent in the studied population. These are risk haplotypes for celiac disease especially when symptoms and diseases related to celiac disease are present. Therefore, it is important to screen patients to investigate a potential diagnosis for celiac disease.

scholarly journals A One-Tube Polymerase Chain Reaction Protocol Demonstrates CC Chemokine Overexpression in Graves’ Disease Glands

1999 ◽  
Vol 84 (8) ◽  
pp. 2873-2882
Author(s):  
Yaqoub Ashhab ◽  
Orlando Dominguez ◽  
Mireia Sospedra ◽  
Carme Roura-Mir ◽  
Anna Lucas-Martín ◽  
...  
Keyword(s):  
Human Leukocyte ◽  
Needle Aspiration ◽  
Graves Disease ◽  
Tissue Samples ◽  
Autoimmune Thyroid ◽  
Leukocyte Antigen ◽  
Cc Chemokine ◽  
Inflammatory Protein ◽  
Cc Chemokines ◽  
Polymerase Chain

An adaptation of mixed oligonucleotide primed amplification of complementary DNA to detect the profile of CC chemokines in biological samples is presented. By introducing normalization, two correction coefficients, performing a single amplification reaction, and five parallel hybridizations, intrasample and intersample comparisons can be reliably made. This protocol of single tube PCR CC chemokine profiling was applied to tissue samples from an autoimmune thyroid condition, Graves’ disease, and from a nonautoimmune condition, multinodular goiter. Results demonstrate overexpression of CC chemokines in Graves’ disease, statistically significant for macrophage inflammatory protein-1α and -1β, which correlated with the aberrant human leukocyte antigen class II expression by thyrocytes, as assessed by flow cytometry. Overexpression of CC chemokines probably plays a major role in determining the characteristics of the lymphocytes migrating to the thyroid gland and influences the course of the disease. The study of chemokine profile should be more informative than the study of isolated chemokines and cytokines, and as it can be applied to fine needle aspiration biopsies, it may be useful to clinical research.

scholarly journals Alemtuzumab-related thyroid disease in people with multiple sclerosis is associated with age and brainstem phenotype at disease onset

2020 ◽  
Vol 6 (2) ◽  
pp. 205521732093392 ◽  
Author(s):  
Siew Mei Yap ◽  
Mary Dillon ◽  
Rachel K Crowley ◽  
Christopher McGuigan
Keyword(s):  
Multiple Sclerosis ◽  
Thyroid Disease ◽  
Chart Review ◽  
Disease Onset ◽  
Human Leukocyte ◽  
Cross Reactivity ◽  
Autoimmune Thyroid ◽  
Leukocyte Antigen ◽  
Younger Age ◽  
Thyroid Medication

Background Autoimmune thyroid disease (AITD) occurs in 40%–50% of alemtuzumab-treated persons with multiple sclerosis (pwMS), most of whom will develop Graves’ Disease (GD). Objective To explore contributory factors for alemtuzumab-related AITD in pwMS. Methods A retrospective patient chart review was performed. Results Sixteen out of 52 (30.8%) pwMS developed AITD. GD occurred in 56.3% ( n = 9), the majority ( n = 7, 77.8%) symptomatic. All but one (85.7%) pwMS with symptomatic GD developed atypical, large and rapid fluctuations in thyroid hormone levels unexplained by effect of anti-thyroid medication alone. All symptomatic GD cases were age ≤32 years when starting alemtuzumab (ɸ = 0.60, p = 0.03). PwMS who started alemtuzumab at a younger age developed thyroid disease earlier ( r = 0.51, p = 0.04). PwMS with clinical and radiological evidence of brainstem involvement at onset of multiple sclerosis were 11 times more likely to develop symptomatic GD compared with those with other phenotypes ( p < 0.01). Conclusion Alemtuzumab-induced reconstitution GD may result from early and increased cross-reactivity between antigens common to the brainstem and thyroid, or presence of shared Human Leukocyte Antigen (HLA) alleles that determine brainstem and thyroid involvement. We suggest cautious use of alemtuzumab in younger (≤32 years) pwMS with early brainstem involvement, especially those actively planning pregnancy, where alternative therapies are readily available.

Beyond the increasing complexity of the immunomodulatory HLA-G molecule

Blood ◽  
2008 ◽  
Vol 111 (10) ◽  
pp. 4862-4870 ◽  
Author(s):  
Edgardo D. Carosella ◽  
Benoit Favier ◽  
Nathalie Rouas-Freiss ◽  
Philippe Moreau ◽  
Joel LeMaoult
Keyword(s):  
Human Leukocyte ◽  
Hematologic Malignancies ◽  
Therapeutic Tool ◽  
Leukocyte Antigen ◽  
Histocompatibility Complex ◽  
Maternal Immune System ◽  
Precise Knowledge ◽  
Mhc Class I Molecule ◽  
Human Leukocyte Antigen G ◽  
Immunomodulatory Function

Abstract Human leukocyte antigen G (HLA-G) is a nonclassic major histocompatibility complex (MHC) class I molecule that functions as an immunomodulatory molecule capable of protecting fetal tissues from the maternal immune system. The relevance of HLA-G in other contexts was investigated soon afterward. Numerous studies have sought (and some have shown) the relevance of HLA-G in pathologic conditions, such as transplantation, autoimmunity, and cancer and hematologic malignancies. One of the main goals of the current research on HLA-G is now to use it in the clinic, either for diagnosis or as a therapeutic tool/target. For this, precise knowledge on the nature and functions of HLA-G is critical. We highlight here what we consider are recent key basic findings on the immunomodulatory function of HLA-G. These strengthen the case for considering HLA-G as clinically relevant.

scholarly journals Significant Association ofHLA-BAlleles and Genotypes in Thai Children with Autism Spectrum Disorders: A Case-Control Study

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Apichaya Puangpetch ◽  
Pongwut Suwannarat ◽  
Montri Chamnanphol ◽  
Napatrupron Koomdee ◽  
Nattawat Ngamsamut ◽  
...  
Keyword(s):  
Neurodevelopmental Disorder ◽  
Human Leukocyte ◽  
Normal Subjects ◽  
Protective Role ◽  
Autism Spectrum ◽  
Thai Population ◽  
Leukocyte Antigen ◽  
Specific Oligonucleotide Probe ◽  
Sequence Specific Oligonucleotide Probe ◽  
The Relationship

Autism is a severe neurodevelopmental disorder. Many susceptible causative genes have been identified. Most of the previous reports showed the relationship between the Human Leukocyte Antigen (HLA) gene and etiology of autism. In order to identifyHLA-Balleles associated with autism in Thai population, we compared the frequency ofHLA-Ballele in 364 autistic subjects with 952 normal subjects by using a two-stage sequence-specific oligonucleotide probe system (PCR-SSOP) method based on flow-cytometry technology.HLA-B⁎13:02(P=0.019, OR = 2.229),HLA-B⁎38:02(P=0.049, OR = 1.628),HLA-B⁎44:03(P=0.016, OR = 1.645), andHLA-B⁎56:01(P= 1.78 × 10−4, OR = 4.927) alleles were significantly increased in autistic subjects compared with normal subjects. Moreover, we found that theHLA-B⁎18:02(P=0.016, OR = 0.375) andHLA-B⁎46:12(P=0.008, OR = 0.147) alleles were negatively associated with autism when compared to normal controls. Both alleles might have a protective role in disease development. In addition, fourHLA-Bgenotypes of autistic patients had statistically significant relationship with control groups, consisting ofHLA-B⁎3905/⁎5801(P=0.032, OR = 24.697),HLA-B⁎2704/⁎5801(P=0.022, OR = 6.872),HLA-B⁎3501/⁎4403(P=0.021, OR = 30.269), andHLA-B⁎1801/⁎4402(P = 0.017, OR = 13.757). This is the first report onHLA-Bassociated with Thai autism and may serve as a marker for genetic susceptibility to autism in Thai population.

scholarly journals Searching for the Autoimmune Thyroid Disease Susceptibility Genes: From Gene Mapping to Gene Function

2003 ◽  
Vol 24 (5) ◽  
pp. 694-717 ◽  
Author(s):  
Yaron Tomer ◽  
Terry F. Davies
Keyword(s):  
Genetic Susceptibility ◽  
Cytotoxic T Lymphocyte ◽  
Twin Studies ◽  
Human Leukocyte ◽  
Epidemiological Data ◽  
Susceptibility Genes ◽  
Autoimmune Response ◽  
Autoimmune Thyroid Diseases ◽  
Autoimmune Thyroid ◽  
Genome Screening

Abstract The autoimmune thyroid diseases (AITD) are complex diseases that are caused by an interaction between susceptibility genes and environmental triggers. Genetic susceptibility, in combination with external factors (e.g., dietary iodine), is believed to initiate the autoimmune response to thyroid antigens. Abundant epidemiological data, including family and twin studies, point to a strong genetic influence on the development of AITD. Various techniques have been used to identify the genes contributing to the etiology of AITD, including candidate gene analysis and whole genome screening. These studies have enabled the identification of several loci (genetic regions) that are linked with AITD, and in some of these loci putative AITD susceptibility genes have been identified. Some of these genes/loci are unique to Graves’ disease (GD) and Hashimoto’s thyroiditis (HT), and some are common to both diseases, indicating that there is a shared genetic susceptibility to GD and HT. The putative GD and HT susceptibility genes include both immune modifying genes (e.g., human leukocyte antigen, cytotoxic T lymphocyte antigen-4) and thyroid-specific genes (e.g., TSH receptor, thyroglobulin). Most likely these loci interact, and their interactions may influence disease phenotype and severity. It is hoped that in the near future additional AITD susceptibility genes will be identified and the mechanisms by which they induce AITD will be unraveled.

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