Addition of immunoglobulin G (IgG) specific for hemoglobin to a solution of hemoglobin results in the formation of a redprecipitate. In contrast, addition of the Fab fragments from this antibody to hemoglobin results in no such precipitate.What could explain this difference in results?Treatment with papain produces Fab fragments with different antigen specificity than the original IgG molecule.IgG can simultaneously bind two different antigens, whereas an Fab fragment can only bind one antigen at a time.The Fab fragments preferentially bind to other Fab fragments rather than to hemoglobin.The hemoglobin molecule antibody-binding sites can bind IgG molecules, but cannot bind Fab fragments.

Antibodies are proteins that are produced by the immune system to recognize and neutralize foreign…

Answered: Addition of immunoglobulin G (IgG)…

Biochemistry

9th Edition

ISBN:9781319114671

Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Publisher:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Chapter1: Biochemistry: An Evolving Science

Section: Chapter Questions

Problem 1P

See similar textbooks

Similar questions

Neutralizing antibodies are effective at preventing infection or toxicity mediated by pathogens or their toxic products. In fact, nearly all vaccines currently in use function by eliciting neutralizing antibodies. One example is the tetanus vaccine, in which neutralizing antibodies are generated against an inactivated form of the tetanus toxin (the tetanus toxoid). The most important feature of a neutralizing antibody is having high affinity for the antigen. being efficient at activating the complement cascade. having a high degree of multivalency, such as being a pentamer or hexamer of immunoglobulin monomers. being present at a high concentration in the circulation. 0 0 0 0
Helper T cells are affected by HIV, how come is this receptor key to the immune system? which line of defense are we referring to? How is it connected to the immune system and which line of defense? Hence, based on your prompt, how are cytokines linked to the defense mechanism of HIV virus? Do you know or can you explain the cascade of events dealing with PAMPS, TLRs, interferon? What do they have to do with the second line of defense?
An immunodeficient mouse strain is identified, that has a single gene defect causing its disease. Mice with this defect have greatly impaired responses to protein antigens following subcutaneous immunization and also exhibit severely delays in the kinetics of their antibody responses. Analysis of their lymph nodes revealed profound alterations in the normal architecture, with a lack of organization of distinct T-cell and B-cell zones. A likely candidate for the defect in these mice is: The chemokine receptor CCR7, which recruits B cells, T cells, and dendritic cells to lymph nodes. The TNF family member LT-b, which is made by Lti cells. The chemokine receptor CXCR5 that recruits B cells to the lymph node follicles. Prox1, the transcription factor required for the development of lymphatic vessels. TNF-a, which is required for the development of FDCs.
Ehrlich's original idea of the selective theory for lymphocyte specificity postulated that a lymphocyte expresses many different antigen-specific receptors, with a foreign antigen or pathogen "selecting" one specific receptor. We now know that the outcome of clonal selection for B cells is the secretion of many copies of the same B-cell receptor in the form of a soluble antibody (humoral immunity). In what specific way was Ehrlich's original theory later refined? What are the challenges to aligning Ehrlich's original model with the above observation of humoral immunity? Does our current model of clonal selection fit this observation any better?
Helper T cells can be activated by macrophages(which engulf everything indiscriminately) or by B cells (which only engulf antigens that stick to their receptors). A. What properties so macrophages and B cells have ibn common that allows them both to activate T cells? B. It has been suggested that macrophages probably do most to fhte T cell activating in the primary response but B cells do most of it in the secondary response. Why does this make sense?
1) 286 individuals were newly diagnosed with Human Immunodeficiency Virus in 2018 in Minnesota. Of these individuals, 76% were male. HIV is an enveloped, ssRNA virus_ Baltimore classification VI. This virus targets CD4+ cells. CD4 refers to a glycoprotein which serves as a co-receptor for T-cells, located on T-helper and T-reg immune cells. a) What part of the HIV virus allows for specificity to CD4+ cells?
It was stated that Rh antigens are so sparsely scattered in the red cell surface that IgG molecules bound to the Rh antigens are too far apart to fix C1q.Therefore, complement-mediated hemolysis cannot be invoked to explain hemolytic disease of the newborn. By what mechanism are the red cells destroyed?
In spite of their low affinity for binding to their antigen, IgM antibodies can be quite effective at promoting the elimination of extracellular bacterial infections. This is due to: The ability of IgM antibodies to traffic across epithelial surfaces Multivalent binding of IgM pentamers to repetitive epitopes on bacterial surfaces The high concentration of IgM antibodies in the serum and in all tissues The early production of IgM antibodies during an immune response The high rate of somatic hypermutation in the genes encoding IgM antibodies
¹C2²2S + E Sk3,0 where S is a T-cell of a particular variety, E is the corresponding (free, i.e. unbound) antigen, and C is a complex consisting of a T-cell bound to an antigen. Ø indicates the loss of T-cells due to decay as described above. 1. Let s, c and e be the concentration of S, C and E, respectively, in the body at time t. Assume that the background exposure to the disease results in a constant concentration eo of the antigen (free or bound) in the body. (b) (c) Consider the T-cell system. Assuming mass action kinetics, write down a system of ODEs for Show that ds dt S + E and k-1 where KM dc dt Show (include your working) that the 2D system of ODEs has two equilibria: (s*,c*) = (0,0) == : -k₁(eo — c)s + k_1c +2k₂c - k3s k-1+k2 k₁ (s*, c*) = ( k₂e0 k3 and KM, eo k2 dt' dt and KM = k₁(eo - c)s - k_1c - k₂c.

Recommended textbooks for you

Biochemistry

ISBN:

9781319114671

Author:

Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Publisher:

W. H. Freeman

Lehninger Principles of Biochemistry

Biochemistry

ISBN:

9781464126116

Author:

David L. Nelson, Michael M. Cox

Publisher:

W. H. Freeman

Fundamentals of Biochemistry: Life at the Molecul…

Biochemistry

ISBN:

9781118918401

Author:

Donald Voet, Judith G. Voet, Charlotte W. Pratt

Publisher:

WILEY

Biochemistry

ISBN:

9781319114671

Author:

Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Publisher:

W. H. Freeman

Lehninger Principles of Biochemistry

Biochemistry

ISBN:

9781464126116

Author:

David L. Nelson, Michael M. Cox

Publisher:

W. H. Freeman

Fundamentals of Biochemistry: Life at the Molecul…

Biochemistry

ISBN:

9781118918401

Author:

Donald Voet, Judith G. Voet, Charlotte W. Pratt

Publisher:

WILEY

Biochemistry

ISBN:

9781305961135

Author:

Mary K. Campbell, Shawn O. Farrell, Owen M. McDougal

Publisher:

Cengage Learning

Biochemistry

ISBN:

9781305577206

Author:

Reginald H. Garrett, Charles M. Grisham

Publisher:

Cengage Learning

Fundamentals of General, Organic, and Biological …

Biochemistry

ISBN:

9780134015187

Author:

John E. McMurry, David S. Ballantine, Carl A. Hoeger, Virginia E. Peterson

Publisher:

PEARSON

SEE MORE TEXTBOOKS