scholarly journals Immunological similarity of thyroid stimulating antibody (TSAb) and thyroid blocking antibody (TBAb) with animal IgG

2012 ◽  
Vol 59 (1) ◽  
pp. 73-79 ◽  
Author(s):  
Yukio Ochi ◽  
Yoshihiro Kajita ◽  
Takashi Hachiya ◽  
Masaru Hamaoki
Keyword(s):  
Blocking Antibody ◽  
Thyroid Stimulating Antibody

scholarly journals Activity of Thyroid Stimulating Antibody and Thyroid Stimulation Blocking Antibody Determined by Radioiodine Uptake into FRTL-5 Cells.

1989 ◽  
Vol 36 (1) ◽  
pp. 55-63 ◽  
Author(s):  
NORIO YOSHIKAWA ◽  
MITSUSHIGE NISHIKAWA ◽  
MASATERU HORIMOTO ◽  
CHISATO UNO ◽  
NORIMICHI TANIGUCHI ◽  
...  
Keyword(s):  
Blocking Antibody ◽  
Radioiodine Uptake ◽  
Thyroid Stimulating Antibody

scholarly journals Changes of TSH-Stimulation Blocking Antibody (TSBAb) and Thyroid Stimulating Antibody (TSAb) Over 10 Years in 34 TSBAb-Positive Patients with Hypothyroidism and in 98 TSAb-Positive Graves’ Patients with Hyperthyroidism: Reevaluation of TSBAb and TSAb in TSH-Receptor-Antibody (TRAb)-Positive Patients

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Nobuyuki Takasu ◽  
Mina Matsushita
Keyword(s):  
Autoimmune Thyroiditis ◽  
Tsh Receptor ◽  
Blocking Antibody ◽  
Receptor Antibody ◽  
Thyroid Stimulating Antibody ◽  
Tsh Receptor Antibody ◽  
Tsh Stimulation

Two TRAbs: TSBAb and TSAb. TSBAb causes hypothyroidism. TSAb causes Graves’ hyperthyroidism. TSBAb and TSAb block TSH-binding to cells as TRAb, measured as TSH-binding inhibitory immunoglobulin (TBII). We reevaluate TSBAb and TSAb. We studied TSBAb, TSAb, and TBII over 10 years in 34 TSBAb-positives with hypothyroidism and in 98 TSAb-positives with hyperthyroidism. Half of the 34 TSBAb-positives with hypothyroidism continued to have persistently positive TSBAb, continued to have hypothyroidism, and did not recover from hypothyroidism. Ten of the 98 TSAb-positives with hyperthyroidism continued to have positive TSAb and continued to have hyperthyroidism. TSBAb had disappeared in 15 of the 34 TSBAb-positives with hypothyroidism. With the disappearance of TSBAb, recovery from hypothyroidism was noted in 13 (87%) of the 15 patients. TSAb had disappeared in 73 of the 98 TSAb-positives with hyperthyroidism. With the disappearance of TSAb, remissions of hyperthyroidism were noted in 60 (82%) of the 73. Two of the 34 TSBAb-positives with hypothyroidism developed TSAb-positive Graves’ hyperthyroidism. Two of the 98 TSAb-positive Graves’ patients with hyperthyroidism developed TSBAb-positive hypothyroidism. TSBAb and TSAb are TRAbs. TSBAb-hypothyroidism and TSAb-hyperthyroidism may be two aspects of one disease (TRAb disease). Two forms of autoimmune thyroiditis: atrophic and goitrous. We followed 34 TSBAb-positive patients with hypothyroidism (24 atrophic and 10 goitrous) over 10 years. All of the 10 TSBAb-positive goitrous patients recovered from hypothyroidism and 19 (79%) of the 24 TSBAb-positive atrophic patients continued to have hypothyroidism.

Sensitive Assay to Detect Thyroid Stimulating Antibody (TSAb) in the Presence of Thyroid Stimulation Blocking Antibody (TSBAb) in Serum

2001 ◽  
Vol 33 (2) ◽  
pp. 115-120 ◽  
Author(s):  
Y. Ochi ◽  
K. Yamashiro ◽  
N. Takasu ◽  
Y. Kajita ◽  
Y. Sato ◽  
...  
Keyword(s):  
Sensitive Assay ◽  
Blocking Antibody ◽  
Thyroid Stimulating Antibody

Thyroid-stimulating antibody and thyrotropin-binding inhibitory immunoglobulin activity in hypothyroid patients who subsequently developed thyrotoxicosis

1990 ◽  
Vol 122 (4) ◽  
pp. 499-504 ◽  
Author(s):  
Hajime Tamai ◽  
Kanji Kasagi ◽  
Osamu Mizuno ◽  
Nobuyuki Kobayashi ◽  
Gen Komaki ◽  
...  
Keyword(s):  
Hypothyroid Patient ◽  
Blocking Antibody ◽  
Autoimmune Thyroid ◽  
Thyroid Stimulating Antibody ◽  
The Third ◽  
Thyroid Stimulating Antibodies ◽  
Antibody Levels ◽  
Blocking Antibodies ◽  
Immunoglobulin Levels ◽  
Hypothyroid Patients

Abstract. Although abnormal thyroid-stimulating and -blocking antibodies have been demonstrated in hyperthyroid and hypothyroid patients with autoimmune thyroid disorders, a direct correlation is not always observed. Thyroid-stimulating antibody, thyrotropinbinding inhibitory immunoglobulin, and thyroid-stimulating blocking antibody levels were determined in three hypothyroid patients who subsequently developed hyperthyroidism. Thyroid-stimulating antibodies levels were normal in one, elevated in another, and unmeasured in the third hypothyroid patient, but became elevated in all patients with the onset of hyperthyroidism. There was discordance, however, in one patient who had markedly elevated thyroid-stimulating antibodies and TSH-binding inhibitory immunoglobulin levels when she was hypothyroid. The data indicate that thyroidal responses to the abnormal stimulating antibodies may differ among patients with autoimmune thyroid disease.

scholarly journals Susceptibility Rather than Resistance to Hyperthyroidism Is Dominant in a Thyrotropin Receptor Adenovirus-Induced Animal Model of Graves’ Disease as Revealed by BALB/c-C57BL/6 Hybrid Mice

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 4927-4933 ◽  
Author(s):  
Chun-Rong Chen ◽  
H. Aliesky ◽  
P. N. Pichurin ◽  
Y. Nagayama ◽  
S. M. McLachlan ◽  
...  
Keyword(s):  
Dominant Gene ◽  
F1 Hybrids ◽  
Graves Disease ◽  
Antibody Activity ◽  
Igg Subclass ◽  
Potential Candidate ◽  
T Helper ◽  
Blocking Antibody ◽  
Thyroid Stimulating Antibody ◽  
A Subunit

Abstract We investigated why TSH receptor (TSHR) adenovirus immunization induces hyperthyroidism more commonly in BALB/c than in C57BL/6 mice. Recent modifications of the adenovirus model suggested that using adenovirus expressing the TSHR A subunit (A-subunit-Ad), rather than the full-length TSHR, and injecting fewer viral particles would increase the frequency of hyperthyroidism in C57BL/6 mice. This hypothesis was not fulfilled; 65% of BALB/c but only 5% of C57BL/6 mice developed hyperthyroidism. TSH binding inhibitory antibody titers were similar in each strain. Functional TSHR antibody measurements provided a better indication for this strain difference. Whereas thyroid-stimulating antibody activity was higher in C57BL/6 than BALB/c mice, TSH blocking antibody activity was more potent in hyperthyroid-resistant C57BL/6 mice. F1 hybrids (BALB/c × C57BL/6) responded to A-subunit-Ad immunization with hyperthyroidism and TSHR antibody profiles similar to those of the hyperthyroid-susceptible parental BALB/c strain. In contrast, ELISA of TSHR antibodies revealed that the IgG subclass distribution in the F1 mice resembled the disease-resistant C57BL/6 parental strain. Because the IgG subclass distribution is dependent on the T helper 1/T helper 2 cytokine balance, this paradigm can likely be excluded as an explanation for susceptibility to hyperthyroidism. In summary, our data for BALB/c, C57BL/6, and F1 strains suggest that BALB/c mice carry a dominant gene(s) for susceptibility to induction of a thyroid-stimulating antibody/TSH blocking antibody balance that results in hyperthyroidism. Study of this genetic influence will provide useful information on potential candidate genes in human Graves’ disease.

Different binding of stimulatory-type and blocking-type TSH receptor antibody with guinea-pig testis membrane

1991 ◽  
Vol 125 (5) ◽  
pp. 563-569 ◽  
Author(s):  
T. Inui ◽  
Y. Ochi ◽  
T. Hachiya ◽  
W. Chen ◽  
Y. Nakajima ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Inhibitory Effect ◽  
Primary Hypothyroidism ◽  
Significant Inhibition ◽  
Tsh Receptor ◽  
Α Subunit ◽  
Blocking Antibody ◽  
Thyroid Stimulating Antibody ◽  
Receptor Antibodies ◽  
Tsh Receptor Antibodies

Abstract. A receptor assay using [125I]bTSH-binding to guinea-pig testis membrane was developed. Unlabelled hCG and FSH inhibited [125I]bTSH binding. In patients with Graves' disease and in untreated hyperthyroid patients, almost all long-acting thyroid stimulators and thyroid-stimulating antibodies, respectively did not inhibit [125I]bTSH binding, which on the other hand was inhibited by thyroid stimulation blocking antibodies in patients with primary hypothyroidism. When the inhibitory effect on the binding of [125I]hCG and 125I-synthetic α-subunit peptide (α26-46) of hCG to testis membrane was examined, bTSH resulted in a significant inhibition. However, all three kinds of TSH receptor antibodies had no inhibitory effect. This study demonstrated 1. interaction of α-subunit of TSH and hCG with the testicular receptor; 2. binding of thyroid stimulation-blocking antibody and lack of binding of thyroid-stimulating antibody to the testicular TSH receptor in spite of binding of these TSH receptor antibodies to the thyroidal TSH receptor, and 3. lack of binding of thyroid-stimulating antibody and thyroid stimulation-blocking antibody to the testicular gonadotropin receptor.

scholarly journals SARS-CoV-2 Entry: At the Crossroads of CD147 and ACE2

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1434
Author(s):  
Claudio Fenizia ◽  
Silvia Galbiati ◽  
Claudia Vanetti ◽  
Riccardo Vago ◽  
Mario Clerici ◽  
...  
Keyword(s):  
Underlying Mechanism ◽  
Membrane Receptors ◽  
Host Cells ◽  
Viral Agent ◽  
Blocking Antibody ◽  
Angiotensin Converting Enzyme 2 ◽  
Host Membrane ◽  
B Virus ◽  
Immunodeficiency Virus

In late 2019, the betacoronavirus SARS-CoV-2 was identified as the viral agent responsible for the coronavirus disease 2019 (COVID-19) pandemic. Coronaviruses Spike proteins are responsible for their ability to interact with host membrane receptors and different proteins have been identified as SARS-CoV-2 interactors, among which Angiotensin-converting enzyme 2 (ACE2), and Basigin2/EMMPRIN/CD147 (CD147). CD147 plays an important role in human immunodeficiency virus type 1, hepatitis C virus, hepatitis B virus, Kaposi’s sarcoma-associated herpesvirus, and severe acute respiratory syndrome coronavirus infections. In particular, SARS-CoV recognizes the CD147 receptor expressed on the surface of host cells by its nucleocapsid protein binding to cyclophilin A (CyPA), a ligand for CD147. However, the involvement of CD147 in SARS-CoV-2 infection is still debated. Interference with both the function (blocking antibody) and the expression (knock down) of CD147 showed that this receptor partakes in SARS-CoV-2 infection and provided additional clues on the underlying mechanism: CD147 binding to CyPA does not play a role; CD147 regulates ACE2 levels and both receptors are affected by virus infection. Altogether, these findings suggest that CD147 is involved in SARS-CoV-2 tropism and represents a possible therapeutic target to challenge COVID-19.

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