During primary infection, complement activation occurs mainly via which pathways before the adaptive response matures?
Explanation
This question distinguishes between the different complement activation pathways and their timing during an immune response. The alternative and lectin pathways are innate and antibody-independent, making them crucial for the early phase of a primary infection.
Other questions
During a primary immune response, what is the typical timeframe for effector cells and molecules of the adaptive response to start clearing the infection?
Which immune effector module is primarily characterized by the actions of group 1 ILCs, TH1 cells, and macrophages in response to intracellular pathogens?
What is the key change in adhesion molecules that allows effector T cells to home to sites of inflammation instead of lymph nodes?
Which cytokine, produced by TH1 cells, is a primary signal for the classical activation of macrophages?
What is the term for the immunological reaction where chronic coordination between TH1 cells and macrophages leads to the formation of a structure that 'walls off' pathogens like Mycobacterium tuberculosis?
Which cytokine, produced by TH2 and ILC2 cells, is known to directly enhance mucus production, smooth muscle contractility, and epithelial cell turnover to help expel helminth parasites?
What is the primary function of the cytokine IL-17, produced by TH17 cells, at sites of infection?
What common subunit is shared by the cytokines IL-12 and IL-23?
The transition of TH17 cells into TH1-type cells, a phenomenon known as T-cell plasticity, is dependent on which cytokine?
What is the primary pathway for the apoptosis of most effector T cells following the clearance of a pathogen, a process known as clonal contraction?
According to a study on individuals vaccinated against smallpox, what is the approximate half-life of the T-cell memory response?
How do secondary antibody responses qualitatively differ from primary responses regarding antibody affinity and isotype?
In the response to Listeria monocytogenes, approximately how many LLO-specific CD4 T cells are present in a naive mouse, and to what number do they expand by day 7 of the infection?
Which cell surface receptor's sustained expression on a subset of effector T cells is indicative of their potential to become long-lived memory T cells?
Which memory T-cell subset is characterized by the expression of the chemokine receptor CCR7 and primarily recirculates through secondary lymphoid organs?
Which cytokine signaling pathway is essential for the long-term survival and proliferation of CD8 memory T cells under normal conditions?
The phenomenon of 'original antigenic sin' describes the tendency of the immune system to do what upon infection with a variant of a previously encountered pathogen?
What is the function of the αE:β7 integrin (CD103), induced on tissue-resident memory (TRM) cells by TGF-beta?
What is the outcome for a primary CD8 T-cell response to Listeria monocytogenes in mice that lack CD4 T cells?
Classically-activated (M1) macrophages are distinguished from alternatively-activated (M2) macrophages by their metabolism of arginine to produce what molecule?
What is the defining characteristic of tissue-resident memory T cells (TRM) that distinguishes them from central (TCM) and effector (TEM) memory cells?
Which combination of cytokines can induce 'noncognate' IFN-gamma production from both TH1 cells and ILC1 cells, independent of T-cell receptor signaling?
What is the primary function of the CD45RO isoform expressed by effector and memory T cells?
During the course of infection with Salmonella, the pathogen downregulates the expression of flagellin and synthesizes new proteins to suppress intracellular killing. This shift in antigen expression causes the T-cell response to change focus. What does this scenario exemplify?
In the experiment tracking the response to LLO from Listeria, the number of memory T cells contracts from about 100,000 at the peak to what approximate number by day 25?
Which of the following describes the immune response to the fungal pathogen Pneumocystis jirovecii in a healthy individual versus an individual with AIDS?
What is the primary role of IL-22 produced by TH17 cells and ILC3s in the context of type 3 immunity?
Which cytokine, produced by pathogen-activated dendritic cells and macrophages, can induce IFN-gamma production in ILC1s and NK cells, promoting early Type 1 responses?
To home to the skin, T cells primed in skin-draining lymph nodes are induced to express an isoform of PSGL-1 known as cutaneous lymphocyte antigen (CLA). What does CLA bind to on cutaneous vascular endothelium?
In the extrinsic pathway of apoptosis that contributes to clonal contraction, the trimerization of Fas (CD95) by FasL leads to the recruitment of which adaptor protein?
Which statement accurately describes the characteristics of memory B cells compared to naive B cells?
What is the primary function of group 2 innate lymphoid cells (ILC2s)?
Which marker is typically absent on effector memory T cells (TEM) but present on central memory T cells (TCM)?
What is the consequence of continuous IL-12 administration for TH1 cells in an infected mouse?
After an initial immunization, functional antigen-specific B-cell memory appears after a delay and reaches its maximum level by what time point?
What is the role of the transcription factor ROR-gamma-t in the context of immune effector modules?
According to Figure 11.25, what is the approximate peak concentration of IgG antibody reached during a tertiary (3rd) immunization?
In addition to CD40L, what other signaling interaction is required for programming optimal CD8 T-cell memory?
Which chemokine receptor and ligand pair is crucial for attracting T cells primed in the GALT back to the small intestine lamina propria?
In mice that lack components of innate immunity but have an intact adaptive immune system, what is the typical course of an infection?
Which cell-surface marker, an isoform of a protein tyrosine phosphatase, is expressed on naive T cells but is replaced by the CD45RO isoform on effector and memory T cells?
What is the primary role of cytokines like TSLP, IL-33, and IL-25, which are produced by epithelial cells in response to helminths?
In addition to their role in destroying infected cells, what other function can effector CD8 T cells perform?
Which statement accurately describes the stability of effector T-cell subsets?
A key difference between ILCs and their corresponding effector CD4 T cell subsets (e.g., ILC1 vs TH1) is that ILCs:
What is the consequence of the high error rate of RNA polymerase used by RNA viruses?
The fusion of several macrophages to form which type of cell is a characteristic feature of granulomas?
According to Figure 11.25, what happens to the affinity of IgM antibodies with repeated immunization?
Which of the following is NOT a mechanism used by TH17 cells to coordinate type 3 responses against extracellular bacteria?